Rutaecarpine Ameliorates Helicobacter pylori-Induced Chronic Atrophic Gastritis by Modulating Macrophage Polarization
10.13359/j.cnki.gzxbtcm.2025.10.028
- VernacularTitle:吴茱萸次碱通过调控巨噬细胞极化改善幽门螺杆菌诱导的慢性萎缩性胃炎
- Author:
Wei XIANG
1
;
Junshan LONG
;
Yutao XIE
;
Yunlong WANG
Author Information
1. 首都医科大学附属北京安贞医院南充医院/南充市中心医院药学部,四川南充 637000
- Keywords:
rutaecarpine;
chronic atrophic gastritis(CAG);
Helicobacter pylori;
macrophage polarization;
NF-κB pathway;
p-p65;
p-IκBα;
rats
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2025;42(10):2556-2563
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the therapeutic effects and underlying mechanisms of rutaecarpine on Helicobacter pylori(Hp)-induced chronic atrophic gastritis(CAG).Methods An Hp-induced CAG rat model was established.Successfully modeled rats were randomly divided into model group,low-dose rutaecarpine group,medium-dose rutaecarpine group,and high-dose rutaecarpine group,with 12 rats in each group.An additional 12 rats served as the normal control group.Body mass changes were recorded before and after treatment.Gastric mucosal histopathology was analyzed using hematoxylin-eosin(HE)staining.Levels of inflammatory cytokines(TNF-α,IL-6,IL-10)in gastric mucosal supernatants were measured by enzyme-linked immunosorbent assay(ELISA).mRNA expression levels of inducible nitric oxide synthase(iNOS),cluster of differentiation 86(CD86),arginase 1(Arg-1),and mannose receptor(CD206)in gastric mucosal tissues were detected by real-time quantitative polymerase chain reaction(RT-qPCR).Protein expression levels of nuclear factor κB(NF-κB)pathway-related proteins were determined by Western Blot.Results Compared with the normal group,the model group exhibited disorganized gastric mucosal epithelium,reduced glandular structures in the lamina propria,significant inflammatory cell infiltration,and elevated gastric mucosal histopathology scores.TNF-α,IL-6,and IL-10 levels in gastric mucosal supernatants,iNOS and CD86 mRNA expression,and phosphorylated NF-κB inhibitor α(p-IκBα)and phosphorylated NF-κB p65 subunit(p-p65)protein levels were significantly increased,while Arg-1 and CD206 mRNA expression were significantly decreased,the difference being statistically significant(P＜0.05).Compared with the model group,medium-and high-dose rutaecarpine treatment reduced inflammatory cell infiltration,restored cellular arrangement,increased glandular structures in the lamina propria,and significantly lowered gastric mucosal histopathology scores,TNF-α,IL-6,and IL-10 levels,iNOS and CD86 mRNA expression,and p-p65 and p-IκBα protein expression were significantly reduced,whereas Arg-1 and CD206 mRNA expression were significantly increased,the difference being statistically significant(P＜0.05),with dose-dependent effects.Conclusion Rutaecarpine ameliorates Hp-induced CAG by modulating macrophage polarization and attenuating inflammatory responses,likely through downregulation of p-p65 and p-IκBα expression and subsequent inhibition of NF-κB pathway activation.
