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Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 in vitro and in vivo

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dc.contributor
dc.contributor.authorDuan Bensong
dc.contributor.authorBao Zhewei
dc.contributor.authorYang Jingya
dc.contributor.authorWang Zhenzhen
dc.contributor.authorLi Aoxiang
dc.contributor.authorYang Jin
dc.contributor.authorLv Mengke
dc.contributor.authorZhang Haibin
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2025-10-28T12:05:50Z
dc.date.available2025-10-28T12:05:50Z
dc.date.issued2025
dc.description.abstractBackground. Astragaloside IV (AS-IV) has demonstrated a protective effect against gastrointestinal tract injury induced by various factors. However, its potential mechanism against chronic atrophic gastritis (CAG) remains unknown. Purpose. The objective of the present study was to investigate the impact of AS-IV on CAG and elucidate its molecular mechanism. Methods. The mRNA and protein levels of protease-activated receptor-1 (PAR-1) and related proteins were assessed using reverse transcription-polymerase chain reaction and western blot analyses, respectively. In addition, the levels of inflammatory factors were measured via enzyme-linked immunosorbent assay in GES-1 cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The CAG model was established in rats induced with MNNG and concurrently treated with AS-IV for 10 weeks. Subsequently, serum samples were collected to assess the expression levels of proteins reflecting inflammatory markers. The gastric tissue sections were used for hematoxylin and eosin staining, immunohistochemical analysis, and the assessment of p-NF-κB p65 and PAR-1 signaling. Results. In-vitro experiments demonstrated that the mRNA levels of PAR-1 were upregulated following treatment with AS-IV and MNNG. Conversely, inhibition of PAR-1 expression reversed the therapeutic effects of AS-IV on MNNG-treated GES-1 cells, leading to increased expression of cyclooxygenase-2 and p-NF-κB p65. In addition, PAR-1 inhibition notably reversed MNNG-induced inflammatory factors, including IL increase. In-vivo experimental validation further confirmed that the upregulation of PAR-1 expression following treatment with AS-IV exerted a protective effect on the gastric mucosa of CAG rats. Conclusion. In conclusion, the findings of the present study suggested that AS-IV exhibited therapeutic efficacy against CAG induced by MNNG; its mechanism may be closely associated with the thrombin/PAR-1 signaling pathway. The present study provides a theoretical foundation for further exploration of the pharmacological effects of AS-IV on the treatment of human CAG
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dc.format.extent10
dc.identifier.citationHistology and Histopathology, Volúmen 40, nº11(2025), 1829-1838
dc.identifier.doihttps://doi.org/10.14670/HH-18-902
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/169809
dc.languageeng
dc.publisherUniversidad de Murcia, Departamento de Histología e Histopatología
dc.relationThe research in this article was funded by NSFC (No. 82200689), The Young Medical Talents Training Program of Shanghai Pudong New Area Health Commission (No. PWRq2023-26) and the Scientific Research Program of Shanghai Pudong New Area Health Commission (the General Program, No. PW2024A-04)
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectChronic atrophic gastritis
dc.subjectMNNG
dc.subjectAstragaloside IV
dc.subjectThrombin
dc.subjectPAR-1
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleAstragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 in vitro and in vivo
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.40, Nº11, (2025)