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Supervisor：

National Administration of Traditional Chinese Medicine
Sponsor：

Institute of Traditional Chinese Medicine，China Academy of Chinese Medical Sciences；China Association of Chinese Medicine

Editor-in-Chief：WU Yiling

Publisher：Editorial Office of Chinese Journal of  Experimental Traditional Medical Formulae

CN：11-3495/R

ISSN：1005-9903（Print）

ISSN：2097-1494（Online）

Composite impact factor：

5.474（CNKI）

Publication Cycle：Semimonthly

Address：No.16，Nanxiao Street，Dongzhimen，Dongcheng District，Beijing

Tel：010-84076882

E-mail：syfjx_2010@188.com

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Exploration of Mechanism of Guipitang on Mitochondrial Biogenesis of Hippocampal Neurons in MMA Rats Based on AMPK/PGC-1α Signaling Pathway

ObjectiveTo investigate the mechanism by which Guipitang regulates mitochondrial biogenesis of hippocampal neurons in methylmalonic aciduria （MMA） rats through the adenosine monophosphate-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1α （AMPK/PGC-1α） signaling pathway.MethodsFifty 5-day-old Wistar rats were randomly divided into a blank group， a model group， a Guipitang group （9.3 g·kg-1）， an AMPK inhibitor group （2.5 mg·kg-1 Compound C）， and a Guipitang + AMPK inhibitor group （9.3 g·kg-1 + 2.5 mg·kg-1 Compound C） using a random number table method. After 3 weeks of administration， the Morris water maze test was used to assess the rats' learning and memory abilities. Hematoxylin-eosin （HE）， Nissl， and terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） staining was performed to detect histopathological changes and apoptosis in rat hippocampal tissue. Colorimetric assays were employed to measure mitochondrial adenosine triphosphate （ATP） content in hippocampal tissue. The mitochondrial superoxide red fluorescent probe method （MitoSOX Red） was used to assess mitochondrial reactive oxygen species （ROS） levels. The JC-1 assay was carried out to detect mitochondrial membrane potential in hippocampal tissue. Transmission electron microscopy （TEM） was conducted to observe pathological changes in mitochondria. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect mitochondrial DNA copy numbers. Western blot was employed to detect AMPK， PGC-1α， phosphorylated AMPK （p-AMPK）， nuclear factor E2-related factor 1 （Nrf1）， nuclear factor E2-related factor 2 （Nrf2）， and mitochondrial transcription factor A （TFAM） in rat hippocampal tissue.ResultsCompared with those in the blank group， rats in the model group exhibited more dispersed movement paths， were unable to locate the platform independently， and had prolonged escape latency， reduced frequency of crossing the platform， significantly reduced time spent in the target quadrant， and significantly increased time spent in the opposite quadrant （P<0.01）. Compared with those in the model group， rats in the Guipitang group and the Guipitang + AMPK inhibitor group had significantly shortened escape latency， significantly increased frequency of crossing the platform， significantly increased time spent in the target quadrant， and significantly reduced time spent in the opposite quadrant （P<0.05， P<0.01）. Compared with the Guipitang group， the AMPK inhibitor group had a longer escape latency， significantly reduced frequency of crossing the platform， significantly reduced time spent in the target quadrant， and significantly increased time spent in the opposite quadrant （P<0.01）. The model group showed disorganized arrangement of hippocampal neurons and nuclear pyknosis. After treatment with Guipitang， the number of regular neurons increased， while the improvement in the Guipitang + AMPK inhibitor group was less than that in the Guipitang group （P<0.01）. Electron microscopy showed that the cristae structure of mitochondria was extensively lost in the model group， but significantly recovered in the Guipitang group （P<0.01）. The Guipitang + AMPK inhibitor group still exhibited mitochondrial membrane rupture and reduced cristae structure. The apoptosis rate was significantly increased in the model group. Compared with the blank group， the model group had significantly increased ROS levels， significantly reduced ATP content， and significantly decreased mitochondrial membrane potential （P<0.01）. Compared with the model group， the Guipitang group had significantly reduced ROS levels， significantly increased ATP content， and significantly increased mitochondrial membrane potential （P<0.01）. Compared with the model group， the Guipitang group showed a significant decrease in apoptosis rate （P<0.01）， and this effect was partially reversed by the AMPK inhibitor （P<0.01）. The model group showed significantly reduced TFAM， PGC-1α， Nrf1， and Nrf2 mRNA expression and protein expression levels （P<0.01）. Compared with the model group， the Guipitang group showed significantly increased TFAM， PGC-1α， Nrf1， and Nrf2 mRNA expression and protein expression levels （P<0.01）. Compared with the blank group， the model group showed significantly reduced p-AMPK/AMPK protein expression levels （P<0.01）. Compared with the model group， the Guipitang group showed significantly increased p-AMPK/AMPK protein expression levels （P<0.01）.ConclusionGuipitang can improve cognitive dysfunction in rats by activating the AMPK/PGC-1α signaling pathway， promoting mitochondrial biogenesis， and alleviating pathological damage to hippocampal neurons.

BAI Huanghuang, ZHENG Hong, LU Xiangpeng

Exploration of Mechanism of Guipitang on Mitochondrial Biogenesis of Hippocampal Neurons in MMA Rats Based on AMPK/PGC-1<italic>α</italic> Signaling Pathway
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Volume 32  Issue 22，2026

    Liuwei Dihuangwan Reduces Valproic Acid-induced ASD-like Behaviors in Rats by Modulating mTOR-mediated Synaptic Plasticity in Prefrontal Cortex-hippocampus Circuit Enhanced Publication

    WU Ji, YIN Niya, OUYANG Lei, HE Siyu, PEI Fangyu, XIE Ying, LI Fan, LEI Qian, ZHAO Sha, ZHANG Di, ZHU Qinquan

    Vol. 32, Issue 22, Pages: 1-11(2026) DOI: 10.13422/j.cnki.syfjx.20251419
    Abstract：ObjectiveTo investigate the effects of Liuwei Dihuangwan on mammalian target of rapamycin （mTOR）-mediated synaptic plasticity in the prefrontal cortex-hippocampus circuit in the rat model of valproic acid （VPA）-induced autism spectrum disorder （ASD） and to explore its potential mechanism for reducing behavioral abnormalities in ASD rats.MethodsThirteen SD pregnant rats were randomized into the VPA group （10 rats） and the control group （3 rats）. On gestational day 13， the VPA group was intraperitoneally injected with VPA solution （600 mg·kg-1）， while the control group was injected with an equal volume of normal saline. Male pups of 21 days old from both groups underwent behavioral tests to screen the ASD model rats （32 rats）. These rats were then randomly assigned to the model （distilled water）， vitamin D （1 480 U·kg-1）， low-dose （0.75 g·kg-1） Liuwei Dihuangwan， and high-dose （1.5 g·kg-1） Liuwei Dihuangwan groups， and normal male pups were selected as the blank group （distilled water）， with 8 rats in each group. Each group was treated with the corresponding drug or an equal volume of distilled water via gavage daily. After drug administration， behavioral tests were conducted again， followed by anesthesia and tissue collection. Nissl staining was carried out to observe the morphological changes of neurons in the prefrontal cortex and hippocampus. Transmission electron microscopy was used to observe changes in hippocampal synaptic structure. Immunohistochemistry and Western blot were employed to determine the expression of mTOR， phosphatidylinositol 3-kinase （PI3K）， and protein kinase B （Akt） in the prefrontal cortex， as well as synaptophysin-1 （SYP-1）， postsynaptic density 95 （PSD95）， and N-methyl-D-aspartate receptors （NMDARs） in the hippocampus.ResultsCompared with the control group， the model group exhibited severe growth retardation and developmental deformities， with abnormal behavioral performance and pathological damage to neurons and synapses in the prefrontal cortex and hippocampus. Compared with the model group， all treatment groups showed reduced behavioral abnormalities and pathological damage to neurons and synapses in the prefrontal cortex and hippocampus， with the most significant effects in the high-dose Liuwei Dihuangwan group. Immunohistochemistry and Western blotting results showed that compared with the control group， the model group exhibited significantly increased protein levels and phosphorylation ratios of p-mTOR， p-Akt， and p-PI3K in the prefrontal cortex （P<0.05， P<0.01）， and decreased protein levels of SYP-1 and PSD95 and increased protein level of NMDARs in the hippocampus （P<0.01）. Compared with those in the model group， the protein levels of p-mTOR， p-Akt， and p-PI3K in the prefrontal cortex decreased in the vitamin D and high-dose Liuwei Dihuangwan groups （P<0.05）， and the p-mTOR/mTOR， p-Akt/Akt， and p-PI3K/PI3K ratios in the prefrontal cortex declined in the vitamin D group （P<0.05）. The high-dose Liuwei Dihuangwan group showed a reduction in p-PI3K/PI3K ratio （P<0.05）. The protein level of SYP-1 and PSD95 in the hippocampus increased in the vitamin D， low-dose Liuwei Dihuangwan， and high-dose Liuwei Dihuangwan groups （P<0.05， P<0.01）， while the protein level of NMDARs decreased in the vitamin D and high-dose Liuwei Dihuangwan groups （P<0.01）.ConclusionLiuwei Dihuangwan significantly reduces VPA-induced ASD-like behaviors and enhances the regeneration and repair of neurons in the prefrontal cortex and synaptic structures in the hippocampus by downregulating of PI3K/Akt/mTOR expression in the prefrontal cortex， upregulating SYP-1 and PSD95 expression in the hippocampus， and inhibiting NMDARs expression.  
    Keywords：Liuwei Dihuangwan;autism spectrum disorder;mammalian target of rapamycin （mTOR） signaling pathway;synaptic plasticity  
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    Mechanism of Wendan Tang Against Atherosclerosis by Regulating Ferroptosis Based on JAK2/STAT3 Signaling Pathway

    QIU Tingting, OUYANG Xiaoqiang, FANG Bangjiang

    Vol. 32, Issue 22, Pages: 12-21(2026) DOI: 10.13422/j.cnki.syfjx.20260563
    Abstract：ObjectiveTo investigate the mechanism through which Wendan Tang ameliorates atherosclerosis （AS） in mice by regulating ferroptosis via the Janus kinase 2（JAK2）/signal transducer and activator of transcription 3 （STAT3） signaling pathway.MethodsTwelve 8-week-old male C57BL/6J mice of SPF grade were selected as the blank control group and fed a standard diet. Additionally， sixty age-matched male apolipoprotein E knockout （ApoE-/-） mice of the same strain and SPF grade were selected and assigned through a random number table into the following groups （n=12 per group）： a model group， a low-dose （3.9 g·kg-1·d-1） Wendan Tang group， a medium-dose （7.8 g·kg-1·d-1） Wendan Tang group， a high-dose （15.6 g·kg-1·d-1） Wendan Tang group， and an atorvastatin calcium （0.01 g·kg-1·d-1） group. All ApoE-/- mice were fed a high-fat diet for the modeling of AS. Starting from week 9， the blank and model groups were administrated with an equal volume of normal saline by gavage， and the remaining groups with corresponding agents by gavage. After 8 weeks of intervention， samples were collected for analysis. Oil red O staining and Masson staining were used to observe lipid deposition in the aorta， and hematoxylin-eosin （HE） staining was employed to examine AS plaque formation. The serum levels of total cholesterol （TC）， triglycerides （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） were measured by an automatic biochemical analyzer. The serum levels of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， superoxide dismutase （SOD）， malondialdehyde （MDA）， and reduced glutathione （GSH） were determined by enzyme-linked immunosorbent assay （ELISA）. The level of Fe2+ in the aortic tissue was measured by ELISA. Western blot was performed to determine the protein levels of JAK2， phosphorylated JAK2 （p-JAK2）， STAT3， phosphorylated STAT3 （p-STAT3）， solute carrier family 7 member 11 （SLC7A11）， and glutathione peroxidase 4 （GPX4） in the aortic tissue. Real-time quantitative polymerase chain reaction （Real-time PCR） was utilized to measure the mRNA levels of JAK2， STAT3， SLC7A11， and GPX4 in the aortic tissue.ResultsCompared with the blank control group， the model group exhibited increased aortic plaque number and area， enhanced lipid deposition， elevated serum levels of TC， TG， LDL-C， TNF-α， IL-6， and MDA （P<0.05， P<0.01）， declined serum levels of HDL-C， SOD， and GSH， and downregulated protein levels of SLC7A11 and GPX4 in the aortic tissue （P<0.05， P<0.01）. The aortic tissue of the model group exhibited an elevated Fe2+ level and upregulated protein levels of p-JAK2 and p-STAT3 and mRNA levels of JAK2 and STAT3 （P<0.05， P<0.01）. Compared with the model group， low-， medium-， and high-dose Wendan Tang， as well as atorvastatin calcium， significantly attenuated these pathological alterations. Specifically， the treatments decreased aortic plaque burden and lipid deposition and lowered serum TC， TG， LDL-C， TNF-α， and MDA levels （P<0.05， P<0.01）. Concurrently， these interventions raised serum HDL-C， SOD， and GSH levels， upregulated the protein levels of SLC7A11 and GPX4 in the aortic tissue （P<0.05， P<0.01）， reduced the Fe2+ level， and downregulated the protein levels of p-JAK2 and p-STAT3 and the mRNA levels of JAK2 and STAT3 in the aortic tissue （P<0.05， P<0.01）.ConclusionWendan Tang ameliorates aortic lesions， dyslipidemia， and oxidative stress， decreased the phosphorylation levels of JAK2/STAT3， and increased the expression of SLC7A11 and GPX4 in the mouse model of AS. The results suggest that the anti-AS effect of Wendan Tang may be associated with the modulation of the JAK2/STAT3 signaling pathway and inhibition of ferroptosis.  
    Keywords：Wendan Tang;atherosclerosis;ferroptosis;Janus kinase 2/signal transducer and activator of transcription 3（JAK2/STAT3） signaling pathway  
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    Lianpo Yin Ameliorates Bile Reflux Gastritis in Rats by Regulating TLR4/NF-κB Signaling Pathway

    XIE Yuqing, CUI Yutian, ZHANG Junna, CAI Chunjiang

    Vol. 32, Issue 22, Pages: 22-30(2026) DOI: 10.13422/j.cnki.syfjx.20260666
    Abstract：ObjectiveTo investigate the ameliorative effect of Lianpo Yin on gastric mucosal injury in the rat model of bile reflux gastritis （BRG） and decipher the underlying mechanism based on the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway.MethodsThirty-six SPF-grade male Sprague-Dawley （SD） rats were randomized into blank， model， hydrotalcite （positive control drug， 0.20 g·kg-1）， NF-κB inhibitor （BAY11-7082， 5.00 mg·kg-1）， low-dose Lianpo Yin （LPY-L， 9.77 g·kg-1）， and high-dose Lianpo Yin （LPY-H， 19.54 g·kg-1） groups （n=6）. Except that the blank group was administrated with distilled water by gavage， the rats in the other groups were induced for the modeling of BRG by gavage with reflux fluid for 35 consecutive days. From the 2nd week of modeling， each treatment group was administrated with the corresponding drugs by gavage 6 h after the end of daily reflux fluid gavage. The BAY11-7082 group received intraperitoneal injection. Meanwhile， the blank group and model group received an equal volume of distilled water by gavage. All interventions were performed for 28 consecutive days. During the experiment period， the general status of rats was observed and body mass changes were recorded， and the stomach index was calculated after the last administration. The histopathological changes of the gastric mucosa were observed under the light microscope after hematoxylin-eosin （HE） staining. The serum levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） were quantified by enzyme-linked immunosorbent assay （ELISA）. The protein levels of TLR4， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65） and IL-6 in the gastric mucosal tissue were determined by Western blot. The nuclear translocation of NF-κB p65 was observed by immunofluorescence （IF） staining.ResultsCompared with the blank group， the model group showed mental depression， retarded body weight gain （P<0.05， P<0.01）， an increased stomach index （P<0.01）， severely damaged gastric mucosal structure with massive inflammatory cell infiltration and intestinal metaplasia （P<0.01）， elevated serum levels of TNF-α and IL-6 （P<0.01）， up-regulated protein levels of TLR4， p-NF-κB p65/NF-κB p65， and IL-6 in the gastric tissue （P<0.01）， and evident nuclear translocation of NF-κB p65 （P<0.01）. Compared with the model group， all drug intervention groups showed improved general status of rats. The body mass of rats in the hydrotalcite group， LPY-L， and LPY-H groups increased （P<0.05）， while the average body mass of rats in the BAY11-7082 group was slightly higher than that in the model group at each time point. All drug intervention groups showed decreased stomach index （P<0.05， P<0.01）， alleviated pathological damage of gastric mucosa with reduced inflammatory cell infiltration （P<0.05， P<0.01）， and declined serum levels of TNF-α and IL-6 （P<0.01）. Hydrotalcite and LPY-L reduced the levels of TLR4 and IL-6 （P<0.05）， but had no significant effect on p-NF-κB p65. LPY-H down-regulated the protein levels of TLR4， p-NF-κB p65/NF-κB p65， and IL-6 and inhibited the nuclear translocation of NF-κB p65 （P<0.01）， with its effect equivalent to that of BAY11-7082 and superior to that of hydrotalcite and LPY-L.ConclusionLianpo Yin can effectively ameliorate gastric mucosal inflammatory injury in BRG rats by inhibiting the activation of the TLR4/NF-κB signaling pathway， reducing the release of downstream pro-inflammatory cytokines， and suppressing the nuclear translocation of NF-κB p65.  
    Keywords：Lianpo Yin;bile reflux gastritis;Toll-like receptor 4/nuclear factor-κB （TLR4/NF-κB） signaling pathway;inflammatory response;gastric mucosal injury  
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