Evidence map›Paper›PMID 40130342›Full record

ArticleHistology and histopathology2025

Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1

Bensong Duan, Zhewei Bao, Jingya Yang, Zhenzhen Wang, Aoxiang Li, Jin Yang, Mengke Lv, Haibin Zhang

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Article in Histology and histopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Bensong Duan *Endoscopy Center, Department of Gastroenterology Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Zhewei Bao *College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Jingya YangCollege of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Zhenzhen WangCollege of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Aoxiang LiCollege of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Jin YangCollege of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Mengke LvCollege of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Haibin ZhangEndoscopy Center, Department of Gastroenterology Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China. haibin_zhang666@163.com.

Funding

NSFC 82200689Scientific Research Program of Shanghai Pudong New Area Health Commission PW2024A-04Young Medical Talents Training Program of Shanghai Pudong New Area Health Commission PWRq2023-26
6 · The paper itself

Abstract

backgroundAstragaloside 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.

methodsThe 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

conclusionIn 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.

Indexed as

Gastritis, AtrophicReceptor, PAR-1SaponinsTriterpenesAnimalsCell LineDisease Models, AnimalGastric MucosaHumansMaleMethylnitronitrosoguanidineRatsRats, Sprague-DawleySignal TransductionUp-Regulationastragaloside AMethylnitronitrosoguanidineReceptor, PAR-1SaponinsTriterpenes

Identifiers

PMID40130342

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.