摘要:ObjectiveTo investigate the potential active ingredients and targets of Baihu Jia Renshentang(BHJRST) for the treatment of obesity combined with type 2 diabetes mellitus(T2DM) by network pharmacology and in vivo experiments.MethodUltra performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry(UPLC-Q-Exactive Orbitrap MS) was used to analyze and identify the material basis of BHJRST. Subsequently, potential targets for the action of the active ingredients were queried in databases such as ChEMBL, Therapeutic Target Database(TTD), YaTCM, DisGeNET and Traditional Chinese Medicine on Immuno-Oncology(TCMIO), and the shared targets were identified by taking the intersection of these targets with disease targets. The shared targets were imported into the STRING database to construct a protein-protein interaction(PPI) network, the hub genes were identified by cytoHubba plug-in, and molecular docking was used to validate the binding energy of the hub genes to the bioactive ingredients in BHJRST. Meanwhile, the shared targets were imported into the DAVID platform for gene ontology(GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis. The predicted results were subsequently verified by animal experiments. Eighteen 8-week-old male skeletal muscle insulin-like growth factor-1 receptor dysfunction(MKR) mice were induced by a high-fat diet for 12 weeks in order to prepare a mouse model of obesity combined with T2DM. The mice were randomly divided into the model group, metformin group(0.2 g·kg-1) and BHJRST group(27 g·kg-1 in raw material), and another 6 male FVB mice of the same age as the normal group. The mice in each group were were given the corresponding drugs by gavage, and the normal and model groups were given the same amount of distilled water by gavage, 1 time/d for 6 consecutive weeks. At the end of administration, the body mass, Lee's index, fasting blood glucose(FBG), oral glucose tolerance test(OGTT) of mice in each group were examined, and the pathological morphology of the white adipose tissue of the epididymis was observed, and the expression of the mRNA of the hub genes in the white adipose tissue of the epididymis was detected by real-time fluorescence quantitative polymerase chain reaction(Real-time PCR).ResultA total of 200 bioactive components of BHJRST were identified, of which 64 bioactive components were reverse-matched to 384 targets, and a total of 308 targets were associated with obesity combined with T2DM. Hub genes included mitogen-activated protein kinase 1(MAPK1), signal transducer and activator of transcription 3(STAT3), MAPK3, interleukin(IL)-2, Janus kinase 1(JAK1), nuclear transcription factor-κB p65(RELA), estrogen receptor 1(ESR1), transcription factor AP-1(JUN), MAPK14 and lymphocyte-specific protein tyrosine kinase(LCK). GO functional annotation showed that it was mainly enriched in cytoplasm, cell membrane and nucleus, and was closely related to important biological processes such as peptide serine phosphorylation, protein phosphorylation and inflammation. In KEGG enrichment analysis, metabolic pathway, lipid and atherosclerosis, phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt) and MAPK signal pathways were significantly enriched. The molecular docking results showed that the hub genes had a stable binding relationship with 10 bioactive components, including quercetin, isoliquiritigenin, and morin, in BHJRST. The results of animal experiments showed that BHJRST could significantly reduce body mass, Lee's index and FBG levels(P<0.01) in mice with obesity combined with T2DM, improve the pathological changes of white adipose tissue, and down-regulate the the mRNA expression of the hub genes in white adipose tissue of the epididymis(P<0.01).ConclusionIn this study, 10 potentially active components such as quercetin, isoliquiritigenin, and morin in BHJRST are identified through network pharmacology and animal experiments, and it is possible to treat obesity combined with T2DM by regulating lipid and atherosclerosis, phosphatidylinositol PI3K/Akt and MAPK signal pathways, which provides important clues and theoretical basis for the study of its mechanism and clinical application.
关键词:Baihu Jia Renshentang;type 2 diabetes;obesity;insulin resistance;network pharmacology;ultra performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry(UPLC-Q-Exactive Orbitrap MS);Hub gene
摘要:ObjectiveTo investigate the effect and mechanism of Taohong Siwutang (TSD) on myocardial ischemia reperfusion injury (MIRI) in ovariectomized (OVX) female mice.MethodAfter the OVX model of female mice was established, the estradiol (E2) level was detected by enzyme-linked immunosorbent assay (ELISA) to verify the model. Sixty OVX mice were randomly divided into six groups: Sham operation group, model group, low, medium, and high dose groups (9, 18, 36 g·kg-1) of TSD, and nuclear factor E2-related factor 2 (Nrf2) inhibitor group, with 10 mice in each group. The MIRI model was verified by a laser speckle flowmeter. The pathological changes in myocardial tissue were detected by 2,3, 5-triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (HE) staining. Serum creatine kinase isoenzyme (CK-MB), cardiac troponin Ⅰ (CTnⅠ), malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels were detected by ELISA. The expression of Nrf2 and heme oxygenase-1 (HO-1) were observed by immunofluorescence staining. The expressions of Nrf2, HO-1, apoptotic B-cell lymphomato-2 (Bcl-2), Bcl-2 associated X protein (Bax), inflammatory cytokines interleukin-18 (IL-18), and interleukin-1β (IL-1β) were detected by Western blot.ResultCompared with the sham operation group, the serum levels of CK-MB, CTnⅠ, MDA, and IL-6 in the model group were increased (P<0.01), and the levels of SOD and IL-10 were decreased (P<0.01). The damage scores of TTC and HE staining in myocardial tissue were increased (P<0.01). The expressions of Nrf2 and HO-1 in myocardial tissue by immunofluorescence were decreased (P<0.01), and the protein expressions of Nrf2, HO-1, and Bcl-2 in myocardial tissue were decreased. The protein expressions of Bax, IL-18, and IL-1β were increased (P<0.01). Compared with the model group, serum levels of CK-MB, CTnⅠ, MDA, and IL-6 of TSD groups were significantly decreased (P<0.05, P<0.01), and SOD and IL-10 were significantly increased (P<0.05, P<0.01). TTC staining and HE staining damage scores of myocardial tissue were significantly decreased (P<0.01). The expressions of Nrf2 and HO-1 in myocardial tissue by immunofluorescence were increased (P<0.01). The protein expressions of Nrf2, HO-1, and Bcl-2 were significantly increased (P<0.05, P<0.01), and those of Bax, IL-18, and IL-1β were significantly decreased (P<0.05, P<0.01). The effect of the high dose group of TSD was the most significant. The serum levels of CK-MB, CTnⅠ, MDA, and IL-6 in the Nrf2 inhibitor group were significantly increased (P<0.05, P<0.01), and the levels of SOD and IL-10 were significantly decreased (P<0.05, P<0.01). The damage scores of TTC and HE staining in myocardial tissue were significantly increased (P<0.01). The expressions of Nrf2 and HO-1 in myocardial tissue by immunofluorescence were significantly decreased (P<0.01). The protein expressions of Nrf2, HO-1, and Bcl-2 in myocardial tissue were significantly decreased, and those of Bax, IL-18, and IL-1β were significantly increased (P<0.01).ConclusionTSD can alleviate MIRI in OVX mice, reduce oxidative stress response and the release of inflammatory factors, and inhibit apoptosis, playing a protective role in OVX mice with MIRI, which may be related to the activation of Nrf2/HO-1 signaling pathway.
摘要:ObjectiveTo investigate the effects of Guizhi Jia Longgu Mulitang on the expression difference of interleukin-10 (IL-10) and tumor necrosis factor -α (TNF-α) in related organs of insomnia rats with sensory dysfunction dominated by lung and study the mechanism of Guizhi Jia Longgu Mulitang in improving insomnia.MethodSD rats were randomly divided into the blank group, model group, western medicine group, and traditional Chinese medicine (TCM) group, with 10 rats in each group. The rats were deprived of sleep by shallow water environment method in a long platform, and the modeling lasted for 42 d. The blank group and model group were given 0.05 mL·kg-1 normal saline by gavage, and the western medicine group and TCM group were given drugs during modeling. To be specific, the western medicine group was given 0.105 mg·kg-1 dexzopiclone tablet by gavage, while the TCM group was given 7 600 mg·kg-1 Guizhi Jia Longgu Mulitang by gavage, both lasting for 28 days. After successful modeling, the Morris water maze experiment was performed on the 42nd day to detect the motion and spatial memory ability of rats. The levels of IL-10 and TNF-α in serum were detected by enzyme-linked immunosorbent assay (ELISA). The protein expression of IL-10 and TNF-α in the lung and brain tissue of rats was detected by Western blot. The levels of IL-10 and TNF-α in the lung and brain tissue of rats were detected by immunohistochemistry.ResultCompared with the blank group, the sleep stages non-rapid eye movement ( NREM ) and rapid eye movement ( REM ) of the model group were significantly shortened (P<0.5, P<0.01), and the wake stage was significantly increased (P<0.01). The total time and distance of platform exploration were significantly increased (P<0.01). In the target quadrant (the third quadrant), the percentage of exploration time and the times of crossing the platform were significantly decreased (P<0.01). ELISA results showed that the serum IL-10 level was significantly decreased (P<0.01), and TNF-α level was significantly increased (P<0.01). The results of Western blot showed that the protein expression of IL-10 in brain and lung tissue of rats was significantly decreased (P<0.01), and the protein expression of TNF-α was significantly increased (P<0.01). The results of immunohistochemistry showed that the expression of IL-10 in the brain and lung tissue of rats was significantly decreased (P<0.01), and that of TNF-α was significantly increased (P<0.01). Compared with the model group, the NREM stage and REM stage of the western medicine group and the TCM group were significantly increased (P<0.5, P<0.01), and the wake stage was shortened (P<0.5). The total time and distance of platform exploration were significantly decreased (P<0.01). In the target quadrant (the third quadrant), the percentage of exploration time and the times of crossing the platform were significantly increased (P<0.05, P<0.01). The serum IL-10 level was significantly increased (P<0.01), and the serum TNF-α level was significantly decreased according to the ELISA results (P<0.01). The results of Western blot showed that the protein expression of IL-10 in brain tissue and lung tissue was significantly increased (P<0.01), and the protein expression of TNF-α was significantly decreased (P<0.01). The results of immunohistochemistry showed that the expression of IL-10 in brain tissue and lung tissue was significantly increased (P<0.05, P<0.01), and the expression of TNF-α was significantly decreased (P<0.05, P<0.01).ConclusionGuizhi Jia Longgu Mulitang can improve the expression of IL-10 and TNF-α in brain and lung tissue of insomnia rats with sensory dysfunction dominated by lung, prolong sleep time, and then improve insomnia. The mechanism may be related to improving the expression level of inflammatory factors.
关键词:Guizhi Jia Longgu Mulitang;sensory dysfunction dominated by lung;insomnia;inflammatory factor;five mind classification diagnosis method of insomnia by traditional Chinese medicine
摘要:ObjectiveTo observe the effect of Scutellariae Radix-Coptidis Rhizoma on plaque stability in atherosclerotic (AS) mice and to explore its possible mechanism of action based on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB) signaling pathway.MethodTen normal C57BL/6J mice were used as the normal group, and the same strain of ApoE knockout (ApoE-/-) mice were fed with a high-fat diet for 12 weeks to construct an atherosclerosis model. Mice were randomly divided into five groups, namely the model group, the atorvastatin group, and the Scutellariae Radix-Coptidis Rhizoma low-, medium-, and high-dose groups, with ten mice in each group. Then normal and model groups were given equal volume of saline gavage, and the low-, medium-, high-dose Scutellariae Radix-Coptidis Rhizoma groups were given 1.95, 3.9, 7.8 g·kg-1 of the drug by gavage for 8 weeks, respectively. The general state of mice was observed. Hematoxylin-eosin staining was utilized to observe the pathology of aortic root plaques and calculate the percentage of plaque area. Masson staining and oil red O staining combined with immunohistochemistry of F4/80 and α-SMA were used to detect the plaque components of aortic root plaques and calculate the plaque vulnerability index. Enzyme-linked immunosorbent assay was adopted to detect the expression levels of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Western blot was applied to detect the protein expression levels of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), TLR4, MyD88, NF-κB p65, and phosphorylation (p) -NF-κB p65 in the aortic tissues of mice in each group. Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) assay was employed to detect the expression levels of MMP-2, MMP-9, TLR4, and MyD88, NF-κB p65 mRNA.ResultCompared with the model group, the general state of the mice in each medication group was improved, and no obvious side effects were observed. Compared with the model group, the percentage of plaque area in the aortic root of AS mice was significantly reduced in the medium- and high-dose Scutellariae Radix-Coptidis Rhizoma groups (P<0.05). The content of collagen fibers and smooth muscle cells in the plaques of the high-dose Scutellariae Radix-Coptidis Rhizoma group was significantly increased (P<0.01), and the content of lipids and macrophages was significantly reduced (P<0.05), the plaque vulnerability index of each dose group of Scutellariae Radix-Coptidis Rhizoma was significantly reduced, with significant reduction of the medium- and high-dose groups (P<0.01). MMP-2 and MMP-9 protein and mRNA expression levels in aortic tissues were significantly reduced in medium- and high-dose Scutellariae Radix-Coptidis Rhizoma groups (P<0.05). The serum levels of TNF-α and IL-6 were significantly reduced in AS mice in medium- and high-dose Scutellariae Radix-Coptidis Rhizoma groups (P<0.05). In the medium- and high-dose Scutellariae Radix-Coptidis Rhizoma groups, the levels of TLR4, MyD88 protein, and mRNA expression in aortic tissues were significantly reduced (P<0.05), and the level of NF-κB p65 phosphorylation in aortic tissues was significantly reduced (P<0.05).ConclusionScutellariae Radix-Coptidis Rhizoma may play an anti-inflammatory and stabilizing role by inhibiting the TLR4/MyD88/NF-κB signaling pathway.
关键词:Scutellariae Radix-Coptidis Rhizoma;atherosclerosis;inflammatory response;vulnerable plaque;Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB);mechanism of action
摘要:ObjectiveTo observe the effect of the combination of total saponin of Astragali Radix-total alkaloids of Nelumbinis Folium on reversal cholesterol transport (RCT) in hyperlipidemia rats, and to discuss its mechanism.MethodSixty SD rats were randomly divided into control group, high-fat diet group, total saponin of Astragali Radix-total alkaloids of Nelumbinis Folium low (17 mg·kg-1+40 mg·kg-1), middle (34 mg·kg-1+80 mg·kg-1), high dose (68 mg·kg-1+160 mg·kg-1) groups and simvastatin (2.1 mg·kg-1) group, with 10 mice in each group. The Hyperlipidemia model was duplicated by feeding rats with a high-fat diet for 6 weeks. From the 3rd week, except for the control group and the high-fat diet group given distilled water, other groups were given corresponding drugs intragastric treatment for 4 weeks. The changes in blood lipid and liver function of rats were detected by an automatic biochemical analyzer. Hematoxylin-eosin (HE) and oil red O staining were used to observe the pathological morphological changes and steatosis of rat liver tissue. The contents of total cholesterol (TC) and total bile acid (TBA) in rat liver tissue and feces were determined by a semi-automatic biochemical analyzer. The mRNA and protein expression levels of peroxisome proliferators-activated receptors γ (PPARγ), liver X receptors α (LXRα), ATP-binding cassette transporter G1 (ABCG1) and cholesterol 7α-hydroxylase (CYP7A1) in rat liver tissue were detected by Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) and Western blot.ResultCompared with the control group, the contents or activities of TC, triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), TBA, aspartate aminotransferase (AST), alanine aminotransferase (ALT) in serum were significantly increased (P<0.01), and the contents of high-density lipoprotein cholesterol (HDL-C) in the high-fat diet group were significantly decreased (P<0.01). The hepatocyte was clearly swollen like ballooning degeneration, with a lot of fat vacuoles and red fat droplets. The contents of TC and TBA in liver tissue and feces were significantly increased (P<0.01), and the mRNA and protein expression levels of PPARγ, LXRα, ABCG1, and CYP7A1 in liver tissue were significantly decreased (P<0.01). Compared with the high-fat diet group, the contents or activities of TC, TG, LDL-C, TBA, AST, and ALT in the serum of rats in administered groups were significantly decreased (P<0.01), while the content of HDL-C was significantly increased (P<0.01). Hepatocyte swelling was significantly reduced, and the ballooning degeneration, fat vacuoles, and red lipid droplets in liver tissue were significantly decreased. The contents of TC and TBA in liver tissue were significantly decreased (P<0.05, P<0.01), and the contents of TC and TBA in feces were significantly increased (P<0.05, P<0.01). The mRNA and protein expression levels of PPARγ, LXRα, ABCG1, and CYP7A1 in liver tissue were significantly increased (P<0.05, P<0.01).ConclusionTotal saponin of Astragali Radix-total alkaloids of Nelumbinis Folium has a positive effect on the prevention and treatment of hyperlipidemia rats, and its mechanism may be related to the activation of PPARγ/LXRα/ABCG1 signaling pathway and regulation of RCT.
关键词:hyperlipidemia;total saponin of Astragali Radix;total alkaloids of Nelumbinis Folium;reverse cholesterol transport;peroxisome proliferators-activated receptors γ (PPARγ)/liver X receptors α (LXRα)/ATP-binding cassette transporter G1 (ABCG1) signaling pathway
摘要:ObjectiveThe human angiotensin converting enzyme2 (hACE2) transgenic mouse model was used to clarify the antiviral efficacy of BD-77 against a novel coronavirus SARS-CoV-2 and explore the action mechanism of BD-77 against SARS-CoV-2.MethodSARS-CoV-2 Omicron and Delta variant strains-infected VeroE6 cell models were established and administered with BD-77 to observe the antiviral effect of BD-77 in vitro. A kit was used to detect the effect of BD-77 in vitro on the binding of spike S protein of SARS-CoV-2 virus (Delta/Omicron) to angiotensin converting enzyme2 (ACE2). Chromatography was adopted to detect the binding of BD-77 to the S protein and N protein of the novel coronavirus. hACE2 transgenic C57BL/6 mice were divided into a blank control group, SARS-CoV-2 infection group, BD-77 administration groups of 37.5 mg·kg-1 and 75 mg·kg-1, with eight mice in each group. The pneumonia model of SARS-CoV-2-infected hACE2 transgenic mice was built to observe the survival of the mice, detect the virus titer of the lung tissue of the mice, and observe the lesions in the lung tissue.ResultBD-77 had a certain inhibitory effect on Omicron and Delta variant strains in vitro, with median inhibitory concentration (IC50) of 526.3 mg·L-1 and 653.0 mg·L-1, respectively. BD-77 had no significant inhibitory effect on the binding of the S protein of WT, Omicron, and Delta variant strains of SARS-CoV-2 to ACE2 and had no binding effect with the S protein and N protein of the novel coronavirus. No mice in the blank group died, while the mortality rate of SARS-CoV-2-infected mice was 75%. There was a large amount of virus replication in the lung tissue of the mice and large areas of inflammatory infiltration in the lung tissue and interstitium. Compared with the model group, BD-77 administration groups of 37.5 mg·kg-1 and 75 mg·kg-1 could reduce the mortality of mice, significantly lower the virus titer in the lung tissue of mice (P<0.05), and improve lung lesions.ConclusionBD-77 demonstrated significant inhibitory effects against SARS-CoV-2 virus in vitro and in vivo. However, its mechanism of action did not involve direct inhibition of the virus itself or intervention in the virus-host binding process. This finding suggests that the mechanism of action of BD-77 needs to be thoroughly investigated and elucidated by further experiments.
摘要:ObjectiveTo observe the therapeutic effect of BD-77 by nebulized inhalation on animal models of various respiratory viral infections and investigate the mechanism of broad-spectrum antiviral action of BD-77 using proteomics.MethodThe influenza virus H1N1/FM1 experiment used ICR mice and divided them into a normal group, model group, Tamiflu group, and BD-77 groups of 75 and 37.5 g·L-1 for inhalation of 20 min and 25 min. Human coronavirus 229E and OC43 experiment divided the BALB/c mice into a normal group, model group, chloroquine phosphate group, and BD-77 groups of 75, 37.5, 18.75, and 9.375 g·L-1, with 10 mice in each group. Influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection-induced pneumonia models were used to detect mouse lung index, and real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the viral load in lung tissue. Enzyme-linked immunosorbent assay (ELISA) was used to detect related inflammatory factors in lung tissue, and proteomics analysis was performed on the lung tissue of OC43-infected mice.ResultCompared with that in the normal group, the lung index of mice in each infection group was significantly increased (P<0.01), and viral nucleic acid could be detected in the lung tissue of mice infected with human coronaviruses 229E and OC43. The levels of interleukin-6 (IL-6), IL-10, and tumor necrosis factor-α (TNF-α) in the lung tissue of mice infected with human coronavirus 229E were all significantly increased (P<0.01). BD-77 could significantly reduce the lung index of mice infected with influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 (P<0.05, P<0.01), cut down the viral load in the lungs of mice infected with human coronaviruses 229E and OC43 (P<0.01), and lower the contents of IL-6, IL-10, and TNF-α in the lung tissue of mice infected with human coronavirus 229E (P<0.01). Proteomics analysis of the lung tissue of OC43-infected mice showed that BD-77 regulated the AMPK signaling pathway, TNF signaling pathway, NOD-like signaling pathway, IL-17 signaling pathway, Forkhead box protein O (FoxO) signaling pathway, transforming growth factor-β (TGF-β) signaling pathway, and other signaling pathways.ConclusionNebulized inhalation of BD-77 is effective in treating pneumonia caused by influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection in mice and may exert its antiviral effects by regulating the balance of cellular metabolism, enhancing the immune function of the host, and attenuating inflammatory responses.
摘要:ObjectiveTo explore host factors interacting with influenza virus nucleoprotein (NP) and study their effects on influenza virus replication, as well as the mechanism of gardenia jasminoides iridoid glycoside (IGE) in inhibiting influenza virus.MethodA yeast two-hybrid system was utilized to screen host factors that interacted with influenza virus NP. Heterogeneous nuclear ribonucleoprotein D0 (HNRNPD), glucosamine-6-phosphate deaminase 1 (GNPDA1), poly(rC)-binding protein 1 (PCBP1), and protein inhibitor of activated signal transducer and activator of transcription (STAT) protein 1 (PIAS1) were validated by immunoprecipitation assay. The effects of PIAS1 and HNRNPD on influenza virus replication were compared by a dual luciferase assay, and the effects of IGE on influenza virus replication were examined in the presence of transfected ribonucleoprotein (RNP) and knockdown of PIAS1. ICR mice were randomly divided into a normal group, model group, oseltamivir phosphate group, and high, medium, and low dose IGE groups, with 10 mice in each group. In addition to the normal group, each group was infected with the influenza A virus FM1 strain by nasal drip to establish a viral pneumonia model. The high, medium, and low dose IGE groups were given drugs of 50, 25, and 12.5 mg∙kg-1 by gavage, and the oseltamivir phosphate group was given the drug of 27.5 mg∙kg-1 by gavage. Equal amounts of distilled water were instilled in the normal and model groups for four consecutive days. Later, protein expression of PIAS1, NP, phosphorylated (p)-STAT3, STAT3, p-STAT1, and STAT1 were detected in the lung tissue by Western blot.ResultIn yeast two-hybrid assays, 16 potential host targets interacting with influenza virus NP were identified. Immunoprecipitation experiments revealed that HNRNPD and PIAS1 could interact with influenza virus NP. The dual luciferase reporter assays found that both PIAS1 knockdown and overexpression significantly affected IAV RNP activity (P<0.05, P<0.01), and the effect of HNRNPD on IAV RNP was not significant. Both high and low dose IGE groups reduced influenza virus replication (P<0.05) and reversed the increase in influenza virus replication caused by the knockdown of PIAS1(P<0.05, P<0.01). The expressions of PIAS1, NP, p-STAT3, p-STAT1, and STAT1 in the lung tissue of infected mice were reduced to different degrees in each IGE group (P<0.05, P<0.01).ConclusionPIAS1 interacts with influenza virus NP and is able to inhibit influenza virus replication. IGE may exert antiviral effects by inhibiting the activity of IAV RNP through the PIAS1/STAT1 pathway.
关键词:protein inhibitor of activated signal transducer and activator of transcription (STAT) protein 1 (PIAS1);influenza A virus;nucleoprotein (NP);gardenia jasminoides iridoid glycoside;ribonucleoprotein
摘要:ObjectiveTo explore the molecular mechanism of Qidi Tangshen prescription (QDTS) in regulating podocyte pyroptosis in diabetes nephropathy (DN).MethodThrough in vivo experiment, db/db mice were divided into the model group, QDTS group (3.34 g·kg-1), valsartan capsule group (10.29 mg·kg-1), with db/m mice serving as the normal control. Each group consisted of 8 mice, and they underwent continuous intervention for 8 weeks. After the last administration, mice were euthanized, and kidney pathological changes were observed. Additionally, the expression levels of pyroptosis-related indicators, including NOD-like receptor protein 3 (NLRP3), Gasdermin D protein (GSDMD), and interleukin-1β (IL-1β) protein, were examined. Through in vitro experiment, mouse podocytes were divided into the normal glucose group (5.5 mmol·L-1 glucose), high glucose group (35 mmol·L-1 glucose), DMSO group (35 mmol·L-1 glucose+200 mg·L-1 DMSO), and QDTS group (35 mmol·L-1 glucose+200 mg·L-1 QDTS freeze-dried powder). After 48 hours of intervention, the expression levels of NLRP3, GSDMD, and IL-1β proteins were measured in podocytes. A drug-ingredient-target-disease interaction network for QDTS in the treatment of DN was constructed by network pharmacology methods. The key signaling pathways regulating podocyte pyroptosis were analyzed, and validation was conducted through in vivo and in vitro experiments.ResultCompared with normal group, glomerular hyperplasia and glomerular basement membrane thickening were observed in model group, and some segments were accompanied by obvious podocellular process fusion. The protein expressions of NLRP3, GSDMD and IL-1β in mouse kidney were increased, the protein expressions of mitogen-activated protein kinase 14 (MAPK14), V-Rel reticuloendotheliosis virus oncogene homology A (RELA) and Caspase-8 in mouse kidney were increased (P<0.05). Compared with model group, kidney pathological injury of mice in QDTS group was significantly reduced, and the expressions of NLRP3, GSDMD and IL-1β in kidney of mice in QDTS group and valsartan group were decreased (P<0.05). The protein expressions of MAPK14, RELA and Caspase-8 in kidney of mice in QDTS group and valsartan group were decreased (P<0.05). Network pharmacology results showed that there were 16 targets for QDTS to regulate DN cell pyrodeath, among which MAPK14, RELA and Caspase-8 were the key targets. Compared with normal glucose group, the protein expressions of NLRP3, GSDMD and IL-1β in high glucose group were increased (P<0.05), and the protein expressions of MAPK14, RELA and Caspase-8 in mouse podocytes were increased (P<0.05). Compared with high glucose group, the expressions of NLRP3, GSDMD and IL-1β in podocytes of mice in QDTS group were decreased (P<0.05), and the expressions of MAPK14, RELA and Caspase-8 in podocytes of mice in QDTS group were decreased (P<0.05).ConclusionQDTS reduces damage to DN podocytes, which is associated with its regulation of the MAPK14/RELA/Caspase-8 signaling pathway and inhibition of podocyte pyroptosis.
摘要:ObjectiveTo observe the effect of Zhengan Xifengtang on blood pressure and fecal microflora of spontaneously hypertensive rats (SHRs).MethodA total of 75 male SHRs aged nine weeks were randomly divided into SHR group, Benazepril group (1.00 mg·kg-1·d-1), high-dose Zhengan Xifengtang group (34.5 g·kg-1·d-1), medium-dose Zhengan Xifengtang group (17.25 g·kg-1·d-1), and low-dose Zhengan Xifengtang group (8.625 g·kg-1·d-1). A total of 15 male Wistar-Kyoto (WKY) rats aged nine weeks were selected as the normal group. The normal group and SHR group were administrated with an equal volume of distilled water for eight weeks. During the administration, the blood pressure of the rats was measured regularly. After the intervention, fresh feces were collected with a sterile frozen storage tube, and 16S amplicon information was collected and analyzed. Plasma, hippocampus, and ileum of rats were collected for ultra-high performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS) detection.ResultZhengan Xifengtang decreased the systolic blood pressure and diastolic blood pressure of SHRs. Compared with the SHR group, Zhengan Xifengtang decreased the diversity of fecal microflora of SHRs. At the phylum level, Zhengan Xifengtang increased the relative abundance of SHR Verrucomicrobia and Actinobacteria and decreased the relative abundance of Synergistetes, Tenericutes, and Candidatus Saccharibacteria. Compared with the SHR group, Zhengan Xifengtang increased the relative abundance of Blautia wexlerae, Fusicatenibacter saccharivorans, and Akkermansia muciniphila and decreased the relative abundance of Clostridium lavalense, Intestinimonas butyriciproducens, Acetatifactor muris, Alloprevotella rava, and Oscillibacter valericigenes. Spearman correlation analysis showed that the systolic blood pressure of rats was negatively correlated with the relative abundance of Ethanoligenens, Aerococcus, Butyrivibrio, Olsenella, Bifidobacterium, Clostridium XIVb, Allobaculum, and Fusicatenibacter and positively correlated with the relative abundance of Alloprevotella. Zhengan Xifengtang increased the contents of plasma, hippocampal 5-hydroxy tryptamine(5-HT), and 5-hydroxyindole acetic acid(5-HIAA) in SHRs and decreased the contents of 5-HT and 5-HIAA in the ileum, and the content of 5-HT in the hippocampus was negatively correlated with that in the ileum.ConclusionZhengan Xifengtang can reduce the blood pressure of SHRs, which may be related to reducing the diversity of SHR microflora, regulating the structure of the microflora, increasing the relative abundance of 5-HT and short-chain fatty acids bacteria, and lowering the relative abundance of pathogenic bacteria related to intestinal inflammation.
摘要:ObjectiveTo explore the protective effect of polysaccharide from Inonotus obliquus (IOP) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.MethodA total of 40 male C57BL/6 mice were randomly divided into normal group, model group, dexamethasone group, and high-dose and low-dose IOP groups, with eight mice in each group. The high-dose and low-dose IOP groups were administered intragastrically with IOP at 20 and 10 mg·kg-1, respectively. The normal group and the model group were intragastrically administered with normal saline in equal volumes, and the dexamethasone group was intraperitoneally injected with dexamethasone phosphate injection of 30 mg·kg-1 for 21 days. An ALI mouse model induced by LPS was constructed, and hematoxylin-eosin (HE) staining, immunofluorescence staining, and blood routine were used to detect pathological damage of lung tissue and blood cell content. Enzyme-linked immunosorbent assay (ELISA) and Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) were used to detect the expression levels of various inflammatory factors. Changes in gut microbiota and plasma differential metabolites in mice were detected using 16S rRNA sequencing and ultra-high performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry (UPLC-Q-TOF-MS).ResultCompared with the model group, the lung tissue lesions of ALI mice were significantly improved after IOP administration, and the spleen and thymus index were dramatically increased (P<0.05, P<0.01). The ratio of wet-to-dry weight of lung tissue was sensibly decreased (P<0.05, P<0.01), and the number of lymphocytes was substantially increased (P<0.05, P<0.01). The number of neutrophils was markedly decreased (P<0.01). The expression level of interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-1β (IL-1β), nuclear factor-κB(NF-κB), and nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) decreased prominently (P<0.05, P<0.01) and the expression level of interleukin-10 (IL-10) increased memorably (P<0.01). The 16S rRNA sequencing results show that IOP can regulate and improve intestinal microbial disorders. The UPLC-Q-TOF-MS results indicate that the treatment of ALI mice with IOP may involve pathways related to mitochondrial, sugar, and amino acid metabolism, such as nucleotide sugar metabolism, histidine metabolism, ubiquinone, and other terpenoid compound-quinone biosynthesis, as well as starch and sucrose metabolism.ConclusionThe improvement of lung tissue lesions and inflammatory response by IOP in ALI mice may be related to maintaining intestinal microbiota balance, regulating mitochondrial electron oxidation respiratory chain, as well as sugar and amino acid metabolism pathways, and affecting the production of related microbial metabolites and tricarboxylic acid cycle metabolites.
关键词:polysaccharide from Inonotus obliquus (IOP);acute lung injury (ALI);gut microbiota;metabolomics
摘要:ObjectiveTo investigate the protective mechanism of Qianyang Yuyin granules (QYYY) on aldosterone-induced podocyte injury.MethodA total of 30 C57BL/6J mice were randomly divided into five groups: control group, model group, QYYY low dose (QYYY-L) group, QYYY high dose (QYYY-H) group, and spironolactone (SPL) group, with six mice in each group. Except for the control group, mice were implanted with osmotic minipumps and injected continuously with aldosterone (300 μg·kg-1·d-1) to induce renal injury. The drug administration group was given low and high doses (2.6, 5.2 g·kg-1·d-1) of QYYY and SPL (18 mg·kg-1·d-1) for 28 days. The renal pathological changes of mice were observed by hematoxylin-eosin (HE) staining and Masson staining. The expression levels of Nephrin, Desmin, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), cleaved Caspase-3, nuclear receptor subfamily 3 group C member 2 (NR3C2), extracellular regulated protein kinases (ERK), and phospho-ERK (p-ERK) in kidney tissue were detected by Western blot. The apoptosis levels of kidney tissue were detected by TdT-mediated dUTP nick and labeling (TUNEL) staining, and the superoxide dismutase (SOD) levels were detected. In vitro, the mice were divided into five groups: Control group, model group (aldosterone concentration of 200 nmol·L-1), QYYY-L group, QYYY medium dose (QYYY-M) group, and QYYY-H group (25, 50, and 100 mg·L-1). The effect of different concentrations of QYYY on the relative viability of aldosterone-induced podocytes was detected by cell proliferation and viability assay (CCK-8). The expressions of Nephrin, Desmin, Bax, Bcl-2, cleaved Caspase-3, NR3C2, and p-ERK/ERK were detected by Western blot. AnnexinV-FITC/PI flow cytometry was used to detect the apoptosis levels of podocytes. Reactive oxygen species (ROS) in podocytes were observed by DCFH-DA.ResultCompared with the control group, the model group showed structural pathological changes and fibrotic conditions in the kidney, increased apoptosis levels (P<0.01), and decreased SOD levels (P<0.01). Aldosterone concentration at 200 nmol·L-1 showed a significant decrease in podocyte activity (P<0.05). Podocytes in the model group showed structural pathological changes, disordered arrangement of intercellular microfilaments, increased apoptosis levels (P<0.01), and increased intracellular ROS levels (P<0.01). The protein expressions of Nephrin, Bcl-2, and p-ERK/ERK in kidney tissue and podocytes were decreased (P<0.05, P<0.01). The protein expressions of Desmin, Bax, cleaved Caspase-3, and NR3C2 were increased (P<0.05, P<0.01). Compared with the model group, QYYY alleviated the structural damage and fibrosis of the kidney, decreased the apoptosis levels (P<0.05, P<0.01), and enhanced the SOD content of the kidney (P<0.05, P<0.01). QYYY improved the activity of podocytes (P<0.05, P<0.01), restored the foot process structure of podocytes, and decreased apoptosis levels (P<0.01) and ROS levels of podocytes (P<0.01). The protein expressions of Nephrin, Bcl-2, and p-ERK/ERK in kidney tissue and podocytes were increased (P<0.05, P<0.01), and the protein expressions of Desmin, Bax, cleaved Caspase-3, and NR3C2 were down-regulated (P<0.05, P<0.01).ConclusionQYYY improves aldosterone-induced podocyte injury by regulating the NR3C2/ROS/ERK pathway.
摘要:ObjectiveThe mechanisms underlying therapeutic efficacies of Detumescence Analgesic Plaster was analyzed based on "effect-target" associations.MethodBased on CNKI and PubMed databases, the chemical components of Artemisia seed, bastard speedwell, and menthol in Detumescence Analgesic Plaster were collected. The capacity of transdermal absorption was predicted based on the Encyclopedia of Traditional Chinese Medicine (ETCM 2.0). Golden Triangle of compounds with Accepted used for candidate target prediction based on the Integrative Pharmacology-based Research Platform of Traditional Chinese Medicine (TCMIP v2.0)according to the similarity of chemical structures. At the same time, the SoFDA data platform was employed to collect the symptoms related to the efficacy of Detumescence Analgesic Plaster and its related genes information. In addition, based on the interaction between the above-mentioned candidate targets and their efficacy-related genes, the "effect-target" interaction network of Detumescence Analgesic Plaster was constructed. The key targets by topological features calculation, and functional mining was carried out to explain the efficacy mechanism of Detumescence Analgesic Plaster.ResultA total of 165 candidate targets were obtained based on ETCM 2.0 and TCMIP v2.0 databases, and symptoms related to the efficacy of clearing heat, detumescence, and relieving pain, as well as 1 744 related genes were collected based on the SoFDA database. Network construction and analysis showed that the core effect targets of Detumescence Analgesic Plaster were mainly involved in regulating the "immune-inflammation" balance of the body and maintaining the homeostasis of material and energy metabolism, blood circulation, and nervous system functions, and they were closely related to the efficacy of this prescription in clearing heat, reducing detumescence, and relieving pain. Among them, the heat clearing group of Detumescence Analgesic Plaster had the functions of heat clearing, detoxifying, antibacteria, and anti-inflammation. The biological function of its key effect target group was related to correcting the imbalance of "immune-inflammation" induced by pathogens. The detumescence group of Detumescence Analgesic Plaster had the functions of reducing water and swelling and resolving hard lumps, and the biological function of its core effect target group was related to improving microcirculation disturbance. The pain relieving group of Detumescence Analgesic Plaster had the functions of removing stasis, promoting blood circulation, and relieving pain, and its core effect target group was related to correcting the nervous system and the disorder of material and energy metabolism.ConclusionThe heat clearing, swelling reducing, and pain relieving effects of Detumescence Analgesic Plaster may be closely related to its act on related candidate targets, so as to correct the imbalance of "nerve-immunity-vascular-axis", regulate neuronal excitability and inflammatory response, and intervene in material and energy metabolism. The relevant research results lay a theoretical foundation for clarifying the advantages of Detumescence Analgesic Plaster and assisting its clinical precise positioning.
摘要:ObjectiveTo investigate the molecular mechanism of action of artemisinin in attenuating asthmatic airway inflammation and airway remodeling through the phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt) signaling pathway.MethodFifty male SD rats were randomly divided into blank group, model group, and low-dose, medium-dose, and high-dose groups of artemisinin, with 10 rats in each group. The ovalbumin (OVA)-induced asthma model of the rats was established, and after successful modeling, the blank group and model group received tail vein injection of 1.0 mL·kg-1 normal saline, while the low-dose, medium-dose, and high-dose groups of artemisinin received tail vein injection of 12.5, 25, and 50 mg·kg-1 artemisinin daily for seven days. Airway resistance was measured by the acetylcholine chloride method. Cell number and species changes in the alveolar lavage fluid of each group were determined by flow cytometry. Morphological changes in airway endothelial tissue were determined by the hematoxylin-eosin (HE) staining method. Apoptosis was determined by CytoTox 96 method, and enzyme-linked immunosorbent assay (ELISA) method was used to determine the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome, interleukin-1β (IL-1β), and interleukin-10 (IL-10) expression. Western blot method was used to detect the (p)-PI3K/p-Akt level in the alveolar bronchial tissue of each group.ResultCompared with the blank group, the total number of cells, total number of macrophages, total number of eosinophils, total number of lymphocytes, and total number of neutrophils were significantly higher in the model group (P<0.05). HE staining showed that the airway mucosa of the rats had obvious edema, and a large number of inflammatory cells were infiltrated (P<0.05). The rate of apoptosis was significantly higher (P<0.05), and the levels of the inflammasome NLRP3, IL-1β, and IL-10 increased significantly (P<0.05). p-PI3K/p-Akt level increased significantly (P<0.05). Compared with the model group, the total number of cells, total number of macrophages, total number of eosinophils, total number of lymphocytes, and total number of neutrophils were significantly decreased after the intervention of artemisinin at low, medium, and high concentrations (P<0.05). HE staining showed that the degree of edema of the airway mucosa of the rats was reduced, and the area of the inflammatory cell infiltration was drastically reduced (P<0.05). The apoptosis rate was significantly reduced (P<0.05), and the levels of the inflammasome NLRP3, IL-1β, and IL-10 decreased significantly (P<0.05). p-PI3K/p-Akt level decreased significantly (P<0.05).ConclusionArtemisinin significantly inhibits NLRP3 inflammasome activation, reduces cellular pyroptosis and inflammatory cell expression, and attenuates airway inflammatory manifestations and airway remodeling in asthmatic rats, which may be related to the regulation of p-PI3K/p-Akt, and the results may provide laboratory insights and basis for the treatment of bronchial asthma with artemisinin.
摘要:ObjectiveTo investigate the effects of licoflavone A on the proliferation and glycolysis of gastric cancer cells in the hypoxic environment.MethodHuman gastric cancer AGS cells were classified into five groups: Normoxia, hypoxia, and low-, medium-, and high-dose (25, 50, 100 μmol·L-1, respectively) licoflavone A. The cells in other groups except the normoxia group were cultured in the environment with 5% O2 for 48 h. The cell counting kit-8 (CCK-8) and colony formation assay were employed to examine the proliferation of AGS cells. Cell migration was detected by the scratch assay. The protein and mRNA levels of hypoxia-inducible factor 1-alpha (HIF-1α), glucose transporter 1 (GLUT1), lactate dehydrogenase A (LDHA), pyruvate kinase M2 (PKM2), and hexokinase Ⅱ (HK2) in AGS cells were measured by Western blotting and real-time quantitative polymerase chain reaction (Real-time PCR), respectively. The corresponding kits were used to determine glucose uptake and HK activity.ResultThe CCK-8 results showed that compared with the hypoxia group, the high- and medium-dose licoflavone A groups showed decreased proliferation rate of AGS cells at the time point of 24 h (P<0.01) and all the licoflavone A groups demonstrated decreased proliferation rate at the time point of 48 h (P<0.01). Compared with the normoxia group, the hypoxia group showed increased number of clone formation of AGS cells (P<0.01), which was decreased after the treatment with licoflavone A at high, medium, and low doses (P<0.01). Compared with the normoxia group, the hypoxia group showed increased migration of AGS cells (P<0.01), which was attenuated by the high, medium, and low doses of licoflavone A (P<0.01). Compared with the normoxia group, the hypoxia group showed up-regulated mRNA levels of GLUT1, LDHA, PKM2, and HK2 (P<0.05, P<0.01). Compared with those in the hypoxia group, the mRNA levels of GLUT1, LDHA, PKM2, and HK2 in the high-dose licoflavone A group, GLUT1, LDHA, and HK2 in the medium-dose licoflavone A group, and HK2 in the low-dose licoflavone A group were down-regulated (P<0.05, P<0.01). The protein levels of HIF-1α, GLUT1, LDHA, PKM2, and HK2 in the hypoxia group were higher than those in the normoxia group (P<0.05, P<0.01). Compared with those in the hypoxia group, the protein levels of HIF-1α, GLUT1, LDHA, PKM2, and HK2 in the high-dose licoflavone A group and HK2 in the medium- and low-dose licoflavone A groups were down-regulated (P<0.05, P<0.01). The glucose uptake and HK activity were elevated in the hypoxia group compared with those in the normoxia group (P<0.01). Compared with the hypoxia group, high-dose licoflavone A decreased the glucose uptake and HK activity, and medium-dose licoflavone A decreased the HK activity (P<0.01).ConclusionLicoflavone A inhibits the proliferation of AGS cells under hypoxic conditions by regulating glycolysis in gastric cancer.
摘要:ObjectiveTo explore the effect of Dingkundan on Qi stagnation and blood stasis syndrome in patients with chronic obstructive pulmonary disease (COPD) at a stable phase.MethodA randomized controlled clinical design method was adopted, and 60 patients who were diagnosed with Qi stagnation and blood stasis syndrome in COPD at a stable phase in the outpatient and inpatient departments of the respiratory department of Guang' anmen Hospital of China Academy of Chinese Medical Sciences from June 2019 to December 2019 were divided into observation group and control group according to 1∶1. During the study period, there was no dropout, loss of follow-up, or exclusion between the two groups. On the basis of both groups receiving traditional Chinese medicine (TCM) lung rehabilitation training, the observation group took Dingkundan 7 g/time orally, twice a day. The control group received oral administration of the same specification of Dingkundan starch simulator of 7 g/time, twice a day. Both groups have a treatment period of 12 weeks. The COPD Assessment Test (CAT), modified Medical Research Council (mMRC), fatigue scale-14 (FS-14), self-rating anxiety scale (SAS), self-rating depression scale (SDS), 6-minute walk distance (6MWD), and pulmonary function before and after treatment were evaluated.ResultAfter treatment, both groups showed improvements in CAT, mMRC, FS-14, SAS scores, and 6MWD (P<0.05). The observation group also showed improvements in SDS scores and lung function indicators (P<0.05). Compared with the control group after treatment, the observation group showed more significant improvement in CAT, FS-14, SAS, SDS scores, and 6MWD (P<0.05).ConclusionDingkundan has a clear therapeutic effect on Qi stagnation and blood stasis syndrome in patients with COPD at a stable phase. It can reduce symptom burden, enhance exercise capacity, and improve psychological status and has the potential to improve lung function.
摘要:ObjectiveTo observe the clinical efficacy of Tongdu Huoxue decoction in the treatment of acute lumbar disc herniation (LDH).MethodA total of 316 patients with acute LDH admitted to the orthopedic outpatient department of Hubei Provincial Hospital of Traditional Chinese Medicine and Honghu City Hospital of Traditional Chinese Medicine from January 2020 to June 2023 were randomly divided into two groups. 156 cases in the control group (two cases with stopped follow-up) were treated with meloxicam tablets, while 153 cases in the observation group (five cases with stopped follow-up) were treated with Tongdu Huoxue decoction. Both groups were treated for three months. The clinical efficacy, McGill Pain Score Scale (SF-MPQ), Oswestry Dysfunction Index (ODI) score, and the Japanese Orthopaedic Association (JOA) scores of the two groups before and after treatment were compared. The serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) of the patients before and after treatment were determined by using enzyme-linked immunosorbent assay (ELISA). The NDI-092 type electromyography-evoked potential instrument was adopted to measure the motor conduction velocity and clinical efficacy of the tibial and common peroneal nerves in patients of the two groups before and after treatment, and the clinical safety of the two groups of patients was compared.ResultAfter treatment, the total effective rate in the observation group was 95.4% (146/153), significantly higher than that in the control group of 76.3% (119/156) (χ2 =23.18, P<0.05). After treatment, both groups showed significant reductions in SF-MPQ and ODI scores, as well as the levels of IL-1β, IL-6, and TNF-α (P<0.05), with the observation group showing a more significant reduction (P<0.05). Both groups showed a significant increase in JOA scores and motor conduction velocities of the tibial and common peroneal nerves after treatment (P<0.05), with the observation group showing a more significant increase (P<0.05).ConclusionTongdu Huoxue decoction can alleviate lumbar and leg pain in acute LDH, improve lumbar spine function, and suppress inflammatory reactions. It is highly safe and is worthy of clinical promotion.
关键词:disc herniation;traditional Chinese medicine therapy;lumbar spine function;inflammatory factors
摘要:ObjectiveTo explore the efficacy and safety of Lianhua Qingwen preparation in the treatment of community-acquired pneumonia (CAP).MethodThe PubMed,Embase,Cochrane Collaboration,CNKI,VIP,and Wanfang Medical Network database (CBM) were systematically searched for all the randomized controlled clinical trials (RCTS) of Lianhua Qingwen Preparation in the treatment of CAP from the establishment of the databases to February 2023. The inclusion criteria were established, and the search results were screened. The risk assessment tool (ROB) scale was used to evaluate the methodological quality of the final included studies, and the R software was used for data integration and meta-analysis.ResultA total of 30 pieces of literature were included,involving 2 800 patients. The combined use of Lianhua Qingwen preparation on the basis of antibiotics and other conventional treatments showed that Lianhua Qingwen preparation could improve the cure rate [relative risk(RR)=1.32,95% confidence interval(95% CI)[1.23,1.42],P<0.000 1)] and shorten the time of fever remission [Mean difference(MD)=-1.45,95% CI [-1.93,-0.97],P<0.000 1],and the duration of fever reduction was divided into general population and special population subgroups. The results showed that Lianhua Qingwan preparation could shorten the duration of fever reduction (general population MD=-1.51,95%CI [-2.07,-0.94],P<0.000 1, special population MD=-1.22,95% CI [-2.16,-0.29],P=0.010 6)and does not increase the incidence of adverse reactions(RR=0.85,95%CI [0.62,1.15],P<0.000 1). After nine pieces of virtual literature with negative results were supplemented by the shear compensation method,the cure rate of CAP by Lianhua Qingwan preparation was still improved (RR=1.20,95%CI [1.13,1.29],P<0.000 1).ConclusionThe application of Lianhua Qingwen preparation on the basis of antibiotics in the treatment of CAP can improve the cure rate and shorten the time of fever reduction.
摘要:ObjectiveBased on spatial metabolomics technology combined with pharmacological indexes, to analyze the mechanism of Fritillariae Cirrhosae Bulbus(FCB) powder in improving bleomycin-induced pulmonary fibrosis in rats.MethodSixty SD rats were randomly divided into five groups, including the blank group, the model group, and high, medium, low dosage groups of FCB. Except for the blank group, rats in all other groups were injected with bleomycin by tracheal injection to establish a pulmonary fibrosis model. Postoperatively, the high, medium and low dosage groups of FCB were administered aqueous solutions of FCB powder at doses of 0.36, 0.18, 0.09 g·kg-1, respectively, continuously for 28 d. The blank and model groups were given an equal volume of distilled water by gavage. After the last administration, lung tissues and blood samples were collected, the pathological conditions of rat lung tissues were comprehensively evaluated by hematoxylin-eosin(HE) and Masson staining, and aerodynamic assisted desorption electrospray ionization mass spectrometry imaging(AFADESI-MSI) was used for MSI of rat lung tissues from different experimental groups. Spatial metabolomics analysis was conducted on the fibrotic areas of lung tissues in the model group and the high dosage group of FCB based on HE staining images. Differential metabolites between groups were screened by orthogonal partial least squares-discriminant analysis(OPLS-DA), with variable importance in the projection(VIP) values>1, t-test P<0.05, and fold change analysis. Metabolic pathway analysis of the identified differential metabolites was performed using Kyoto Encyclopedia of Genes and Genomes(KEGG). Protein expression levels of nuclear transcription factor-κB p65(NF-κB p65) and heme oxygenase-1(HO-1) in rat lung tissues were detected by Western blot. Biochemical assessments of superoxide dismutase(SOD), malondialdehyde(MDA) and glutathione(GSH) levels in rat lung tissues were conducted. Serum levels of interleukin(IL)-1β, IL-6, nuclear factor erythroid 2 related factor 2(Nrf2), and tumor necrosis factor-α(TNF-α) were measured by enzyme linked immunosorbent assay(ELISA), and some of the screened signaling pathways with strong correlation were verified.ResultThe results of MSI experiment showed that after 28 d of the administration of FCB powder to rats with pulmonary fibrosis, the content of L-arginine in the fibrotic regions of lung tissues was significantly different from that of rats in the model group, and the content of phosphatidylcholine was lower than that in the fibrotic region of lung tissues of rats in the model group. Western blot results confirmed that, in comparison to the model group, oral administration of FCB powder for 28 d could inhibit the elevated expression of NF-κB p65 protein in the lung tissues of rats with pulmonary fibrosis. Furthermore, high dose of FCB powder was able to significantly inhibit the expression of HO-1 after oral administration (P<0.05). The cytokine detection results indicated that the concentrations of IL-1β, IL-6 and TNF-α in the serum of rats from the high, medium, low dosage groups of FCB were reduced by comparing with the model group, and the high dose of Chuanbeimu powder administered by gavage could significantly inhibit the trend of decreased SOD, GSH, Nrf2 contents and increased MDA content induced by bleomycin.ConclusionOral administration of FCB powder has the potential to partially ameliorate bleomycin-induced pulmonary fibrosis in rats, and its mechanism may be related to the regulation of pathways associated with inflammation(NF-κB p65) and oxidative stress(Nrf2/HO-1).
摘要:ObjectiveTo explore the interaction between bruceoside B and gut microbiota and the inhibitory activity of its metabolites on human lung cancer A549 cells, and to explore the value of bruceoside B in the treatment of non-small cell lung cancer(NSCLC).MethodBruceoside B was co-incubated with the human gut microbiota under anoxic conditions in vitro, and ultra high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry(UPLC-Q-TOF-MS) was used to analyze the metabolic transformation products. Cell counting kit-8(CCK-8) assay was performed to determine the effects of bruceoside B and its metabolites on the proliferation of human lung cancer A549 cells and the half inhibitory concentration(IC50) was calculated. Five healthy male rats were gavaged with bruceoside B(2 mg·kg-1) for 7 days after adaptive feeding. The feces of rats were collected before and after administration. 16S rRNA sequencing was used to assess gut microbiota.ResultBruceoside B was mainly metabolized to brusatol by human gut microbiota, the IC50 of bruceoside B and the conversion product to A549 cells were 1 755.50, 19.57 μmol·L-1, respectively, and the conversion product had a better activity at inhibiting A549 cells proliferation than bruceoside B. Additionally, The results of intestinal flora analysis showed no significant differences in α diversity and β diversity of gut microbiota after administration. In terms of species abundance, at the phylum level, bruceoside B decreased the relative abundance of Actinobacteriota and Proteobacteria, increased the relative abundance of Firmicutes, Patescibacteria and Cyanobacteria. At the genus level, bruceoside B decreased the relative abundance of Staphylococcus, Aerococcus and Psychrobacter, increased the relative abundance of Romboutsia, Lactobacillus, Clostridium sensu stricto 1, Norank-f-norank-o-Clostridia-UCG-014, Turicibacter, Allobaculum and Candidatus Saccharimonas. The results of functional prediction showed that the gut microbiota functional compositions were relatively stable.ConclusionBruceoside B can be deglycosylated by intestinal flora and converted into brusatol, with a significant increase in antitumor activity. The administration of bruceoside B will not cause significant changes in the structure and function of the intestinal flora, resulting in intestinal microecological balance disorders, and the administration appears to be beneficial to the intestinal flora of NSCLC patients.
摘要:In this paper, the name, origin, medicinal parts, producing area, harvesting, processing methods and efficacy of Equiseti Hiemalis Herba(EHH) in famous classical formulas were examined by reviewing related ancient and modern literature. Through textual research, Muzei was first appeared in Zhenyuan Guanglifang(《贞元广利方》), and used as a mainstream name by later generations. It is also known by other names, such as Cuocao and Bigancao. The main origin of ancient EHH was Equisetum hyemale, which was mixed with E. ramosissimum during the Qing dynasty. The medicinal part was the above-ground part of EHH. In ancient times, the genuine producing area was considered to be Qinzhou, which is now Tianshui city, Gansu. In modern times, EHH produced in Liaoning province is believed to be of higher quality. Currently, the main producing area of EHH circulating in the market is the northeast region in China. EHH with stems that are thick and long, a green color, a thick texture, and clearly visible edges and roughness, but without any easily separating joints being considered the best. The processing methods of the past dynasties mainly included filing, removing knots, stir-baked the crude drugs into black on outside and brown in inside, urine soaking, sun drying and shade drying. In modern times, the main processing method is to first moisturize the plant material, and then cut it into sections before drying. In terms of medicinal properties, EHH is considered by both ancient and modern medicine to have a neutral nature, a slightly sweet and bitter taste, and is non-toxic. Its primary therapeutic effects are related to treating eye diseases, intestinal wind bleeding and uterine bleeding. Based on the research, it is suggested that the dried above-ground part of E. hiemale be used in the development and utilization of famous classical formulas. For the processing requirements are not indicated, it is suggested using raw decoction pieces as medicine, and the processing method refers to the 2020 edition of Chinese Pharmacopoeia. If it is clearly stated that fried charcoal is required, it is recommended to refer to general requirements 0213 of the 2020 edition of Chinese Pharmacopoeia, if it is clearly stated that removing knots is required, it is recommended to follow the ancient method.
关键词:famous classical formulas;Equiseti Hiemalis Herba;herbal textual research;origin;medicinal part;producing area;harvesting;processing of traditional Chinese medicine
摘要:Zhuye Shigaotang is one of the 100 classic prescriptions published by the National Administration of Traditional Chinese Medicine. This study used the traceability method and bibliometrics method to analyze the main applicable syndromes, efficacy and meanings, modern disease spectrum, and other aspects of Zhuye Shigaotang, so as to further promote the research and development of this prescription. The results showed that Zhuye Shigaotang originated from the Treatise on Febrile Diseases, and its ingredients included Lophatheri Herba, Gypsum Fibrosum, Pinelliae Rhizoma, Ophiopogonis Radix, Ginseng Radix et Rhizoma, Glycyrrhizae Radix et Rhizoma, and Oryza sativa. The main applicable syndromes of Zhuye Shigaotang recorded in ancient books included heatstroke, cough and asthma, sores, sweat syndrome, hiccup, insomnia, malaria, headache, blood syndrome, nasosinusitis, laryngitis, etc., involving diseases of internal medicine, surgery, gynecology, and pediatrics. Its pathogenesis was "incomplete residual heat, both Qi and Yin injuries, and stomach-Qi disharmony". The research found that Zhuye Shigaotang could also be used to treat acne, measles, and cholera, and it was especially suitable for the treatment at the later stage of epidemic diseases. Lophatheri Herba and Gypsum Fibrosum in the prescription could clear away heat and relieve vexation. Ginseng Radix et Rhizoma,Ophiopogonis Radix, Ginseng Radix et Rhizoma, and Oryza sativa could promote body fluid production and invigorate Qi. Pinelliae Rhizoma could harmonize the stomach and stop vomiting. The prescription had stable compatibility and had the effects of clearing away heat, relieving vexation, invigorating Qi, promoting body fluid production, and harmonizing the stomach. Zhuye Shigaotang was widely applied in modern clinical practices, with high application frequency in the digestive system, pediatric-related diseases, respiratory system, infectious diseases, circulatory system, and neuropsychiatric system. The specific symptoms included recurrent aphtha, hiccup, infantile pneumonia, infantile summer fever, unexplained fever, upper respiratory tract infection, epidemic hemorrhagic fever, and late measles.
摘要:ObjectiveTo investigate the influence of concentration ratio(CR) between the internal reference and target components on the quantitative accuracy of quantitative analysis of multi-components by single marker(QAMS) by taking ginsenosides as an example.MethodUltra performance liquid chromatography(UPLC) was employed, the contents of nine components in Ginseng Radix et Rhizoma(ginsenosides Rg1, Re, Rf, Rh1, Rb1, Rc, Rb2, Rb3, Rd) were determined by external standard method(ES). Using ginsenoside Rg1 as the internal reference, the contents of the remaining 8 ginsenosides were determined by QAMS, and the quantitative results were compared with those of ES to evaluate the quantitative accuracy of the established QAMS. According to the contents of these 9 ginsenosides, the simulated sample solutions with different CRs of ginsenoside Rg1 to ginsenosides Rf, Rb2, Rd were prepared with the reference substance(CR=100∶1, 10∶1, 5∶1, 2∶1, 1∶1, 0.5∶1, 0.25∶1), in order to validate the effect of the CRs between the internal reference and other components on the quantitative accuracy of the QAMS.ResultThe results of ginsenosides Re, Rf, Rb1, Rc, Rb2 calculated by the two methods were the same with the relative standard deviation(RSD)<3%, however, the results of ginsenosides Rh1, Rb3 and Rd calculated by the two methods were different with RSDs of 7.06%-9.61%. According to the result of the simulated sample solution, the difference between the calculated results of ES and QAMS was large when the CR between the internal reference(ginsenoside Rg1) and other components was 5 or 10 or even higher.ConclusionThe quantitative error of QAMS will increase when the CR between the quantitative component and the internal reference is too large, so it is suggested that when establishing the QAMS, the components with close concentration to the internal reference should be selected for quantification.
关键词:multicomponent quantitative analysis;quantitative analysis of multi-components by single marker(QAMS);concentration difference;ginsenoside;quantitative accuracy;ultra performance liquid chromatography(UPLC);Ginseng Radix et Rhizoma
摘要:The comorbidities of vertebrobasilar dolichoectasia(VBD) and cerebral small vessel disease(CSVD) increase the poor prognosis of patients,and elucidating the mechanism underlying their comorbidities helps to explore effective treatment strategies. Therefore,based on the collateral disease theory and combining with the pathogenesis and research progress of traditional Chinese and Western medicine on the understanding of the two,this study proposes that both the disease locations are in the brain collaterals and the pathogenesis is deficiency in foundation and excess in symptoms. The main pathogenesis roots in the deficiency of original Qi and the emptiness of brain collaterals,which corresponds to the dysfunction of endothelial cells and neuro-endocrino-immune networks in modern medicine. The symptoms are cerebral blood stasis,occlusion of cerebral arteries and toxic lesion of cerebral arteries,corresponding to cerebrovascular atherosclerosis,hemodynamic changes,hypoperfusion and toxic metabolites-induced injury of white matter in modern medicine. Based on the collateral disease theory,exploring the common pathogenesis of the VBD and CSVD is expected to facilitate the establishment of TCM treatment scheme including the principles,methods and medicines,and improve the clinical prognosis of patients.
关键词:collateral disease theory;collaterals;vertebrobasilar dolichoectasia;cerebral small vascular disease
摘要:The education concepts of four famous traditional Chinese medicine(TCM) doctors(XIAO Longyou, SHI Jinmo, KONG Bohua and WANG Fengchun) in Beijing during the Republic of China were compared, the commonalities in their education concepts of TCM were sorted out, and the root system of the cultivation and growth of talents in TCM, as well as the direction and way of further development were searched, so as to improve the quality of the inheritance and development of TCM. Based on the systematic review of text and opinion method(SrTO) developed by the centre for evidence-based health care at the Joanna Briggs Institute(JBI) in Australia, this study was conducted to collate and analyze the relevant information, including 14 books, 115 journal papers and 7 documents. Related theory construction and practice of early tutor and academic education have been summarized from college, continuing and tutor education, academic research, examination, and so on. And then the connections and commonalities between the different forms of education in the period were summarized to form a SrTO-based narrative, opinion, text assessment and review instrument(NOTARI) summary table. The findings revealed that these four esteemed TCM doctors and educators, through their substantial influence on TCM education in Beijing, emphasized the importance of classics in teaching and clinical practice, underscored the cultivation of virtue, preserved the traditional teaching model, and championed the establishment of TCM schools. They also put forward novel requisites for the compilation of curricula, teaching materials, and books. Moreover, they advocated for a unified perspective on TCM and western medicine, fostering talent capable of bridging the gap between the two. They encouraged the standardization of TCM teaching examination system, and actively participated in scientific research and book writing. The four TCM doctors transcended the traditional boundaries of TCM practice, fostering a new TCM model of education-clinical-research, and profoundly influencing the contemporary TCM colleges and teacher education.
关键词:traditional Chinese medicine educator;XIAO Longyou;SHI Jinmo;KONG Bohua;WANG Fengchun;republic of China;educational concept
摘要:Tumor metastasis is the major cause of death for tumor patients and the key bottleneck of clinical treatment. In recent years, basic and clinical studies have recognized that tumor microenvironment (TME) is highly correlated with tumor metastasis, which provides hope for anti-metastatic drug development and clinical treatment. At present, the mainstream studies on TME represented by immune checkpoint inhibitors (ICIs) mainly focus on the rectification of immune function of T cells and B cells. However, a large number of studies have shown that the significance of other members of TME for tumor metastasis cannot be ignored, which greatly reflects the progress of anti-metastatic research based on TME regulation. This review focused on tumor metastasis, summarized the mechanism of action of non-T and non-B immune cells [tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs)] and non-immune members [vascular endothelial cells (ECs), tumor-associated fibroblasts (CAFs), and blood platelet] in the process of tumor metastasis in TME based on the literature over the recent five years, and explored their key value in the treatment of metastasis. At the treatment level, this review focused on the perspective of the integration of frontier and traditional methods and took the functional homeostasis remodeling of TME as the entry point to summarize the activity and mechanism of traditional Chinese medicine (TCM) regulation of non-T and non-B immune cells and non-immune members and highlight its advantages and characteristics in clinical intervention of metastasis. This review helps to break through the limitations of over-reliance on T and B immune cells in anti-metastatic research, make the research rely on a wider range of cell groups, explore the potential value of TME in anti-metastatic drug intervention, and enrich the idea and strategy of understanding the anti-metastatic pharmacological activity. The review is also expected to provide a broader vision for the research and development of new anti-metastatic drugs.
关键词:tumor metastasis;tumor microenvironment;tumor immunomodulation;traditional Chinese medicine (TCM) anti-metastatic pharmacology
摘要:Breast cancer has become the malignant tumor with the highest incidence rate. Although the emergence of new drugs has prolonged the overall survival of breast cancer patients, it still possesses a high recurrence and metastasis rate due to tumor heterogeneity and drug resistance. Glucose is the main source of energy metabolism for breast cancer cells, and the glucose metabolism of breast cancer cells is significantly different from that of normal breast cells. The high energy demand and rapid growth of breast cancer cells make their demand for glucose much higher than that of normal cells. Moreover, even under aerobic conditions, the glycolytic effect of breast cancer cells will be significantly enhanced to meet the high energy metabolism demand of breast cancer cells. The main reason for the enhanced glycolytic effect of breast cancer cells is the enhanced activity of glycolysis-related enzymes and regulatory factors, including pyruvate kinase, hexokinase, phosphofructokinase, lactate dehydrogenase, and glucose transporter protein. The metabolism process of glycolysis in breast cancer cells can be regulated by interfering with the activity of these enzymes and regulatory factors, thus inhibiting the proliferation of breast cancer, promoting apoptosis, and reversing drug resistance, invasion, and metastasis. Traditional Chinese medicine (TCM) has a long history of treating breast cancer and has made significant achievements in the aspects of anti-recurrence, metastasis, and drug resistance. In recent years, more and more research related to the intervention of aerobic glycolysis in breast cancer by TCM monomers, single-flavored TCM, and compounds has been conducted and has made great achievements. In addition, a large number of in vivo and in vitro experiments have shown that aerobic glycolysis is an important potential target for the treatment of breast cancer by TCM, but there is a lack of a comprehensive review and summary. On this basis, this paper elaborated on the roles of key targets in aerobic glycolysis and breast cancer and summarized the relevant studies on the treatment of breast cancer by intervention of glycolysis with TCM, with a view to providing new ideas for further research.
关键词:breast cancer;aerobic glycolysis;Warburg effect;traditional Chinese medicine
摘要:Myocardial fibrosis (MF) is a prevalent pathological process in a spectrum of cardiac conditions, including myocardial infarction, hypertensive heart disease, and dilated cardiomyopathy. It is marked by an overabundance of extracellular matrix deposition, diminished myocardial compliance, and impaired cardiac function, which can lead to arrhythmias and sudden cardiac death. The current therapeutic approach primarily aims to suppress the progression of fibrosis, yet the therapeutic outcomes are poor. The pathogenesis of MF involves multiple signaling pathways, including the transforming growth factor-beta (TGF-β)/Smads signaling pathway, nuclear factor-kappa B (NF-κB) signaling pathway, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, and mitogen-activated protein kinase (MAPK) signaling pathway. Traditional Chinese medicine (TCM) boasts a rich history in the treatment of cardiovascular diseases, offering distinctive benefits such as minimal side effects and high safety, and it has demonstrated promising therapeutic effects in the treatment of MF. In recent years, research has turned its attention to the application of TCM in modulating the signaling pathways associated with MF. It has been demonstrated that TCM can modulate the MF-related signaling pathways to exert anti-inflammatory effects, regulate cellular autophagy, cell proliferation, and apoptosis, reduce myocardial oxidative stress and damage, and inhibit the activation of fibroblasts and collagen synthesis, thereby exhibiting the potential to mitigate or even reverse the progression of MF. Experimental research and clinical observations indicate that TCM formulas such as Yixin Futing decoction, Luhong prescription, Zhilong Huoxue Tongyu capsules, and Kangjian Yixin prescription can effectively ameliorate MF and enhance cardiac function through the multi-component regulation of multiple cellular pathways. Specific TCM constituents, including isoliquiritigenin and astragaloside, have been shown to inhibit the expression of TGF-β1, thereby disrupting the Smad signaling pathway. Compounds like glycyrrhizic acid and allicin can suppress the NF-κB signaling pathway and curtail collagen synthesis in myocardial cells, and forsythoside can activate the PI3K/Akt signaling pathway, contributing to its anti-fibrotic effects.
关键词:myocardial fibrosis;traditional Chinese medicine;signaling pathways;research progress
摘要:Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in memory and cognitive function. Despite some achievements in AD research over the past few decades, its exact etiology remains elusive, with no reliable treatment currently available. This has spurred an urgent need for novel therapeutic strategies, particularly for neuroprotective agents with minimal side effects and high efficacy. Natural plant extracts contain a class of steroidal or triterpenoid saponin compounds, exhibiting various pharmacological activities, and they are believed to hold immense potential in the prevention and treatment of AD. Studies have indicated that natural saponins may exert their effects through multiple pathways, including reducing amyloid-β peptide deposition, inhibiting abnormal phosphorylation of Tau protein, modulating oxidative stress, decreasing inflammatory responses, and suppressing cell apoptosis. Particularly, certain traditional Chinese medicine (TCM) formulations containing natural saponin components have demonstrated promising advantages in AD treatment, offering significant clinical prospects. This review summarized the research progress on saponin compounds extracted from natural plants in the prevention and treatment of AD and delved into their mechanisms of action. Through comprehensive analysis of these studies, the potential mechanisms of saponins in AD treatment were elucidated, aiming to provide valuable insights for the development of novel therapeutic drugs, and the review hopes that future research and clinical experiments will fully explore their potential in AD treatment, offering more effective therapeutic options for patients.
关键词:Alzheimer's disease;triterpenoid saponins;steroidal saponins;mechanism of action
摘要:Ischemic cardiovascular and cerebrovascular diseases, encompassing ischemic heart disease and ischemic cerebrovascular disease, possess the features of high prevalence, disability, and mortality rates, thus ranking as the leading cause of global mortality. The shared etiology of ischemic heart disease and ischemic cerebrovascular disease involves local hypoperfusion caused by vascular stenosis, atherosclerosis, and infarction. Their intricate pathological processes involve various mechanisms such as inflammation, pyroptosis, apoptosis, and autophagy. However, interventions targeting individual pathological pathways offer limited therapeutic effects. There is an urgent need to explore novel treatment strategies or medications capable of simultaneously intervening in multiple pathological pathways. Mesenchymal stem cells, through their paracrine effects, play a role in tissue repair, with exosomes playing an important role. Mesenchymal stem cell-derived exosomes exhibit immunomodulatory and reparative properties similar to their parent cells while also reducing the side effects and infusion toxicity associated with the direct application of stem cells. Thus, they hold broad prospects for the treatment of ischemic cardiovascular and cerebrovascular diseases. Traditional Chinese medicine (TCM) and formulations, with their characteristics of multiple components, targets, and multi-level system regulation, can improve the cellular microenvironment by modulating mesenchymal stem cell-derived exosomes, thereby exerting therapeutic effects on ischemic cardiovascular and cerebrovascular diseases. This viewpoint highlights the concept of microscopic pattern differentiation in modern TCM and represents another significant area of TCM modernization. This article provided a comprehensive overview of the therapeutic effects and mechanisms of mesenchymal stem cell-derived exosomes in ischemic cardiovascular and cerebrovascular diseases while discussing the application of TCM in regulating mesenchymal stem cell-derived exosomes in ischemic cardiovascular and cerebrovascular diseases, offering new insights for the prevention and treatment of ischemic cardiovascular and cerebrovascular diseases using TCM.
关键词:traditional Chinese medicine;mesenchymal stem cells;exosomes;ischemic heart disease;ischemic cerebrovascular disease
摘要:This article reviews relevant literature on the prevention and treatment of cancer with hesperidin published in the past 10 years by searching electronic databases such as China National Knowledge Infrastructure(CNKI), Wanfang, and PubMed, and summarizes the research progress on the anticancer mechanism of hesperidin. Hesperidin has a wide range of pharmacological effects, including anti-inflammatory, antioxidant, antibacterial, antiviral, anticancer, immune-regulatory, anti-radiation, neuroprotective and cardiovascular protective properties and so on. Its anticancer mechanisms mainly include inhibiting cancer cell proliferation, promoting apoptosis, reducing angiogenesis, inhibiting invasion and migration of cancer cells, regulating immunity and autophagy, and exerting antioxidant and anti-inflammatory effects. As a broad-spectrum anticancer drug, hesperidin manifests chemo-preventive and therapeutic effects across various cancers, contingent upon its multifaceted anticancer mechanisms. Furthermore, this article summarizes the synergistic effects of hesperidin in combination with cisplatin, doxorubicin, cyclophosphamide and paclitaxel. It elucidates that hesperidin can enhance the cytotoxicity of these anticancer drugs against cancer cells while mitigating drug resistance and adverse side effects. Nonetheless, the clinical use is somewhat constrained due to its poor water solubility and limited bioavailability. Therefore, this article also outlines the current strategies for enhancing hesperidin's bioavailability, including structural modification, combination with other chemical substances, and utilization of nano drug carriers.The discovery of derivatives of hesperidin not only preserves the anticancer efficacy of hesperidin, but also effectively overcomes the shortcomings of poor water solubility and low bioavailability of hesperidin, effectively predicting the good application prospects of hesperidin and its derivatives.
关键词:hesperidin;derivatives;anti-cancer;mechanism of action;research progress
摘要:Alzheimer's disease (AD) is a neurodegenerative disease with progressive losses of memory and cognitive function as the main clinical manifestations. It is difficult to be cured because of the complex pathogenesis. Histone acetylation regulates gene transcription and chromosome structure remodeling without changing the coding sequences of genes, participating in the pathological process of AD via modulating the amyloid beta-protein (Aβ) deposition, Tau phosphorylation, neuron growth, and synaptic plasticity. Traditional Chinese medicine can prevent and control AS via multiple targets and pathways from a holistic view. Animal and cell experiments have proven that traditional Chinese medicine can attenuate AD by regulating histone acetylation. Focusing on the key role of histone acetylation in AD, this study reviews the relevant studies in the last five years from the aspects of active ingredients of traditional Chinese medicine and traditional Chinese medicine compound prescriptions. The available studies suggest that the main mechanisms involve antagonizing apoptosis, inhibiting oxidative stress, ameliorating Tau and Aβ deposition, maintaining synaptic function, nourishing neurons, and repairing myelin sheath. The treatment methods include invigorating kidney and tranquilizing mind, tonifying spleen and harmonizing middle energizer, and opening orifices and resolving phlegm. The commonly used herbal medicines in compound prescriptions include Poria, Glycyrrhizae Radix et Rhizoma, Chuanxiong Rhizoma, Acori Tatarinowii Rhizoma, and Paeoniae Radix Alba. The findings indicate that traditional Chinese medicine demonstrates great potential in the prevention and treatment of AD, providing a theoretical basis for the clinical treatment and research of AD.
关键词:Alzheimer's disease;histone acetylation;traditional Chinese medicine;mechanism;research progress
摘要:The persistent,difficult-to-treat,and recurrent abdominal pain,diarrhea,and mucinous bloody stools that characterize ulcerative colitis (UC) are indicative of an inflammatory bowel disorder. The cause of the sickness remains uncertain,and the outcome of modern medical treatment is not encouraging. The incidence of UC has been steadily increasing over time,making it essential to discover novel treatments in clinical practice. For centuries,traditional Chinese medicine (TCM) has been a successful method for preventing and curing this malady. In the original text of Shanghanlun, ZHANG Zhongjing repeatedly discussed symptoms similar to UC,such as diarrhea,chronic dysentery,intestinal wind,and visceral toxins. The effective formulas proposed in Shanghanlun have laid the groundwork for the later use of TCM for treatment of UC. Research in recent times has revealed the distinct benefits of TCM in both relieving the symptoms and improving the quality of life of UC patients. Banxia Xiexintang,a compound of this type,has been found to be effective in network pharmacology,molecular docking,clinical observation,and animal experiments,and its therapeutic effects have been considerable in the treatment of UC. Extensive experiments have revealed a strong correlation between the effectiveness of Banxia Xiexintang in treating UC and factors such as inflammatory cytokines,intestinal microbiota,immune responses,related signaling pathways, and pyroptosis. This article presents a comprehensive examination of Banxia Xiexintang for treatment of UC,encompassing its theoretical basis,drug composition,and mechanism of action. This paper is expected to provide more theoretical support for clinical application of Banxia Xiexintang.
摘要:Viral hepatitis is an important cause of liver cirrhosis and liver cancer, which has become a major public health problem in the world. Traditional Chinese medicine has unique advantages in treating viral hepatitis, which can inhibit virus replication and enhance immunity. It can effectively prevent liver fibrosis and canceration, improving liver function and symptoms significantly with definite clinical curative effects, a high level of safety, and seldom drug resistance. In addition, it reduces the side effects of western medicine, achieving the effect of synergy and attenuation while reducing the recurrence rate of patients after drug withdrawal. Attention has been paid to the research on the treatment of viral hepatitis with traditional Chinese medicine, and great progress has been made in experimental research and clinical practice. In this paper, the research progress of traditional Chinese medicine in the treatment of viral hepatitis at home and abroad in recent five years was systematically reviewed. Modern research has confirmed that traditional Chinese medicine can play a role in the treatment of viral hepatitis by directly or indirectly inhibiting the virus, anti-inflammatory, anti-fibrosis, anti-oxidation, regulating immunity, regulating autophagy, and other signal pathways. In clinics, traditional Chinese medicine compound or combined with western medicine is often adopted to ameliorate the clinical symptoms of patients such as fatigue and loss of appetite, improve the immune mechanism of the body, enhance the antiviral ability, shorten the treatment course of patients and improve their quality of life. The research provides a reference for pharmacological research, clinical research, and new drug development for viral hepatitis.
关键词:viral hepatitis;Chinese medicine treatment;pharmacological research;clinical research