Erkundung der Stabilität der alveolaren Epithelzellen in der idiopathischen Lungenfibrose basierend auf der Milz als Verteidiger und den Mechanismen der Behandlung mit chinesischer Medizin

  • role: First author第一作者
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

  • Email:542277060@qq.com
  • Introduction:陈杰,博士,助理研究员,从事中医肺系及免疫性疾病基础和临床研究,E-mail:542277060@qq.com
CHEN Jie1,  
  • Affiliation:

    Affiliated Hospital of Liaoning University of TCM,Shenyang 110032,China

PANG Lijian2,  
  • Affiliation:

    Affiliated Hospital of Liaoning University of TCM,Shenyang 110032,China

ZANG Ningzi2,  
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

WANG Jingyu1,  
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

LI Siyu1,  
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

LIANG Yuanyu1,  
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

XU Xinzhu1,  
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

LEI Ping1,  
  • role: Corresponding author通信作者
  • Affiliation:

    Liaoning University of Traditional Chinese Medicine(TCM),Shenyang 110847,China

  • Email:deanoftcm@126.com
  • Introduction:吕晓东,博士,教授,主任医师,从事中医肺系疾病基础和临床研究,E-mail:deanoftcm@126.com
LYU Xiaodong1*

Resümee

Die idiopathische Lungenfibrose (IPF) kann der Kategorie der pulmonalen Netzwerkerkrankungen zugeordnet werden, und ihr pathogenetischer Mechanismus liegt hauptsächlich in der verlorenen Lufternährung, dem Verlust des negativen Netzwerks und der Bildung von Blutgerinnseln im zentralen Netzwerk. Der Mangel an Luft und Negativität ist die grundlegende Pathologie, die sich durch IPF zieht, und die Behinderung des Netzwerkblutes ist ein Schlüsselfaktor in der Krankheitsentwicklung, während der Verlust der Milz als Verteidiger eng mit dem pathogenetischen Muster des pulmonalen Netzwerks geschwächt durch Blut verbunden ist. Der Begriff Milz als Verteidiger stammt ursprünglich aus dem Klassischen Inner Book Yellow, wo eine gesunde Milz eine vollständige Abwehr bedeutet, positive Energie intern gespeichert ist, das Böse nicht eindringen kann und sein Konzept große Ähnlichkeiten mit der immunabwehrenden Funktion der modernen Medizin aufweist. Wenn die Milz als Verteidiger ihre Funktion verliert, können anomaliehafte Veränderungen in der Struktur und Funktion der Epithelbarriere der Lungenbläschen auftreten und mit einer Vielzahl von angeborenen Immunzellen interagieren, um den Entzündungs- und Fibro​​seprozess zu fördern. Daher behandelt diese Studie die Erschöpfung der Immunität der Epithelbarriere der Lungenbläschen (AECs) und deren Interaktion mit angeborenen Immunzellen sowie die Anwendung chinesischer Immuntherapie zur Stärkung der Milz als Verteidiger und zur Behandlung von IPF durch Anhebung der Luftfeuchtigkeit. Dies stärkt nicht nur die wissenschaftliche Bedeutung der Milz als Verteidiger in den Mechanismen der IPF-Entwicklung, sondern bietet auch neue Forschungsrichtungen und -perspektiven für die zukünftige klinische Behandlung.

Schlüsselwort

Milz als Verteidiger, pulmonales Netzwerk geschwächt durch Blut, idiopathische Lungenfibrose, zelluläre Stabilität, alveoläre Epithelzellen

References

  1. 1.
    RICHELDI L,COLLARD H R,JONES M G.Idiopathic pulmonary fibrosis[J].Lancet,2017,389(10082):1941-1952.
  2. 2.
    PODOLANCZUK A J,THOMSON C C,REMY-JARDIN M,et al.Idiopathic pulmonary fibrosis:State of the art for 2023[J].Eur Respir J,2023,61 (4):2200957.
  3. 3.
    BONELLA F,SPAGNOLO P,RYERSON C.Current and future treatment landscape for idiopathic pulmonary fibrosis[J].Drugs,2023,83(17):1581-1593.
  4. 4.
    PENG F F,JAING J H,BAO Y J,et al.Analysis of the marketing of rare disease drugs in China based on the First Batch of Rare Disease Catalog[J].China Pharmacy,2024,35(11):1291-1295.
  5. 5.
    ZHANG A Q,WAN J Y,YAO H Q.Exploring the mechanism and clinical application of intestinal mucosal immunity in the intervention of phlegm-dampness constitution regulation based on the theory of "spleen being in charge of the defensive function"[J].J Beijing Univ Tradit Chin Med,2023,46(2):159-163.
  6. 6.
    WAN J S,LIU T.Analysis of YE Tianshi's Xinrun Tongluo Zethod[J].Chin J Basic Med Tradit Chin Med,2024,30(4):569-571.
  7. 7.
    LI H R,WU Y L.Inheritance and innovation of luobing research[J].J Nanjing Univ Tradit Chin Med,2022,38(12):1075-1085.
  8. 8.
    PAN J X,LYU X D,P[ANG L J,et al.Effectof tonifying lung and dredging collateral method to treat idiopathic pulmonary fibrosis based on theory of lung collateral disease[J].Chin Arch Tradit Chin Med,2020,38(8):86-89.
  9. 9.
    WANG J Y,WANG J R,PANG L J,et al.Exploration on pathological basis of "accumulation in Qi collateral,stasis in blood collateral" in idiopathic pulmonary fibrosis based on epithelial mesenchymal transformation and the idea of treating[J].Chin Arch Tradit Chin Med,2022,40(8):179-182.
  10. 10.
    YU R Z,PANG L J,WANG T J,et al.Differentiation and treatment on idiopathic pulmonary fibrosis from deficiency,toxin,phlegm and stasis[J].China J Tradit Chin Med Pharm,2022,37(10):5815-5818.
  11. 11.
    LIU Y T,LYU X D,PANG L J,et al.Modern medicine basis of dredging and supplementing collaterals method reversing the pathogenesis of idiopathic pulmonary fibrosis with lung deficiency and collateral stasis syndrome[J].J Tradit Chin Med,2017,58(16):1381-1384.
  12. 12.
    PHAN T,PALIOGIANNIS P,NASRALLAH G K,et al.Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis[J].Cell Mol Life Sci,2021,78(5):2031-2057.
  13. 13.
    HEWLETT J C,KROPSKI J A,BLACKWELL T S.Idiopathic pulmonary fibrosis:Epithelial-mesenchymal interactions and emerging therapeutic targets[J].Matrix Biol,2018,71-72:112-127.
  14. 14.
    LIU T,GONZALEZ DE LOS SANTOS F,ZHAO Y,et al.Telomerase reverse transcriptase ameliorates lung fibrosis by protecting alveolar epithelial cells against senescence[J].J Biol Chem,2019,294(22):8861-8871.
  15. 15.
    QI X,LUO Y,XIAO M,et al.Mechanisms of alveolar type 2 epithelial cell death during acute lung injury[J].Stem Cells,2023,41(12):1113-1132.
  16. 16.
    MOSS B J,RYTER S W,ROSAS I O.Pathogenic mechanisms underlying idiopathic pulmonary fibrosis[J].Annu Rev Pathol,2022,17:515-546.
  17. 17.
    ENOMOTO Y,KATSURA H,FUJIMURA T,et al.Autocrine TGF-β-positive feedback in profibrotic AT2-lineage cells plays a crucial role in non-inflammatory lung fibrogenesis[J].Nat Commun,2023,14(1):4956.
  18. 18.
    MARCONI G D,FONTICOLI L,RAJAN T S,et al.Epithelial-mesenchymal transition (EMT):The type-2 EMT in wound healing,tissue regeneration and organ fibrosis[J].Cells,2021,10(7):1587.
  19. 19.
    OLAJUYIN A M,ZHANG X,JI H L.Alveolar type 2 progenitor cells for lung injury repair[J].Cell Death Discov,2019,5:63.
  20. 20.
    Shirvaliloo M.The blood-gas barrier in COVID-19:an overview of the effects of SARS-CoV-2 infection on the alveolar epithelial and endothelial cells of the lung[J].Tissue Barriers,2021,9(4):1937013.
  21. 21.
    ZOU J,LI Y,YU J,et al.Idiopathic pulmonary fibrosis is associated with tight junction protein alterations[J].Biochim Biophys Acta Biomembr,2020,1862(5):183205.
  22. 22.
    WIENER-KRONISH J P,ALBERTINE K H,MATTHAY M A.Differential responses of the endothelial and epithelial barriers of the lung in sheep to Escherichia coli endotoxin[J].J Clin Invest,1991,88 (3):864-875.
  23. 23.
    CONFORTI F,RIDLEY R,BRERETON C,et al.Paracrine SPARC signaling dysregulates alveolar epithelial barrier integrity and function in lung fibrosis[J].Cell Death Discov,2020,6:54.
  24. 24.
    ZHANG L,WANG Y,WU G,et al.Macrophages:Friend or foe in idiopathic pulmonary fibrosis?[J].Respir Res,2018,19(1):170.
  25. 25.
    ISSHIKI T,VIERHOUT M,NAIEL S,et al.Therapeutic strategies targeting pro-fibrotic macrophages in interstitial lung disease[J].Biochem Pharmacol,2023,211:115501.
  26. 26.
    ARABPOUR M,SAGHAZADEH A,REZAEI N.Anti-inflammatory and M2 macrophage polarization-promoting effect of mesenchymal stem cell-derived exosomes[J].Int Immunopharmacol,2021,97:107823.
  27. 27.
    WARHEIT-NIEMI H I,HUIZINGA G P,EDWARDS S J,et al.Fibrotic lung disease alters neutrophil trafficking and promotes neutrophil elastase and extracellular trap release[J].Immunohorizons,2022,6(12):817-834.
  28. 28.
    PAPAYANNOPOULOS V.Neutrophil extracellular traps in immunity and disease[J].Nat Rev Immunol,2018,18(2):134-147.
  29. 29.
    SHA H X,LIU Y B,QIU Y L,et al.Neutrophil extracellular traps trigger alveolar epithelial cell necroptosis through the cGAS-STING pathway during acute lung injury in mice[J].Int J Biol Sci,2024,20(12):4713-4730.
  30. 30.
    KIM M K,KIM J.Properties of immature and mature dendritic cells:Phenotype,morphology,phagocytosis,and migration[J].RSC Adv,2019,9(20):11230-11238.
  31. 31.
    BOCCHINO M,ZANOTTA S,CAPITELLI L,et al.Dendritic cells are the intriguing players in the puzzle of idiopathic pulmonary fibrosis pathogenesis[J].Front Immunol,2021,12:664109.
  32. 32.
    VIVIER E,ARTIS D,COLONNA M,et al.Innate lymphoid cells:10 years on[J].Cell,2018,174(5):1054-1066.
  33. 33.
    LIU B,JIANG Q,CHEN R,et al.Tacrolimus alleviates pulmonary fibrosis progression through inhibiting the activation and interaction of ILC2 and monocytes[J].Int Immunopharmacol,2024,132:111999.
  34. 34.
    GIESECK R L,WILSON M S,WYNN T A.Type 2 immunity in tissue repair and fibrosis[J].Nat Rev Immunol,2018,18(1):62-76.
  35. 35.
    SHAN H,ZHENG X,LI M.The effects of Astragalus membranaceus active extracts on autophagy-related diseases[J].Int J Mol Sci,2019,20(8):1904.
  36. 36.
    TANG Z,HUANG G.Extraction,structure,and activity of polysaccharide from Radix Astragali[J].Biomed Pharmacother,2022,150:113015.
  37. 37.
    ZHANG R,XU L,AN X,et al.Astragalus polysaccharides attenuate pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition and NF-κB pathway activation[J].Int J Mol Med,2020,46(1):331-339.
  38. 38.
    YANG C G,MAO X L,WU J F,et al.Amelioration of lung fibrosis by total flavonoids of astragalus via inflammatory modulation and epithelium regeneration[J].Am J Chin Med,2023,51(2):373-389.
  39. 39.
    JAIN R,HUSSEIN M A,PIERCE S,et al.Oncopreventive and oncotherapeutic potential of licorice triterpenoid compound glycyrrhizin and its derivatives:Molecular insights[J].Pharmacol Res,2022,178:106138.
  40. 40.
    BAI Y,GAO L,HAN T,et al.18β-glycyrrhetinic acid ameliorates bleomycin-induced idiopathic pulmonary fibrosis via inhibiting TGF-β1/JAK2/STAT3 signaling axis[J].J Steroid Biochem Mol Biol,2024,243:106560.
  41. 41.
    LEE I S,KANG K S,KIM S Y.Panax ginseng pharmacopuncture:Current status of the research and future challenges[J].Biomolecules,2019,10(1):33.
  42. 42.
    ZHONG K,HUANG Y,CHEN R,et al.Author correction:The protective effect of ginsenoside Rg1 against sepsis-induced lung injury through PI3K-Akt pathway:Insights from molecular dynamics simulation and experimental validation[J].Sci Rep,2024,14(1):21205.
  43. 43.
    ZHAO Y,WU C.Establishment and research progress of food pharmacy[J].China J Chin Mater Med,2011,36(4):391-395.
  44. 44.
    WANG D,GONG L,LI Z,et al.Antifibrotic effect of Gancao Ganjiang decoction is mediated by PD-1/TGF-β1/IL-17A pathway in bleomycin-induced idiopathic pulmonary fibrosis[J].J Ethnopharmacol,2021,281:114522.
  45. 45.
    LIANG Y,YAN Y,LIU N,et al.Shengxian decoction improves lung function in rats with bleomycin-induced idiopathic pulmonary fibrosis through the inhibition of PANoptosis[J].J Ethnopharmacol,2024,329:118153.
  46. 46.
    YAN Y N,LIANG Y L,WANG J P,et al.Improvement of lung function in rats with idiopathic pulmonary fibrosis by shengxiantang via regulating cell senescence mediated by Wnt3a/β-catenin signaling pathway[J].Chin J Exp Tradit Med Form,2024,30(12):31-38.
  47. 47.
    FENG Z L.To investigate the intervention mechanisms of Yifei Jianpi Recipe on idiopathic pulmonary fibrosis in rats based on wnt3a/β-catenin signaling pathway[D].Lanzhou:Gansu University of Chinese Medicine,2023.

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