Investigating Effect of Xianglian Huazhuo Prescription on Cell Cycle and Proliferation in Rats with Chronic Atrophic Gastritis Through TGF-β1/Smads Signaling Pathway
10.13422/j.cnki.syfjx.20241316
- VernacularTitle:基于TGF-β1/Smads信号通路探讨香连化浊方对慢性萎缩性胃炎大鼠细胞周期和增殖的影响
- Author:
Yican WANG
1
;
Jie WANG
1
;
Yirui CHENG
1
;
Xiaojing LI
1
;
Yibin MA
1
;
Qiuhua LIU
1
;
Ziwei LIU
1
;
Yuxi GUO
1
;
Pengli DU
1
;
Yanru CAI
1
;
Yao DU
1
;
Zheng ZHI
1
;
Bolin LI
1
;
Qian YANG
1
Author Information
1. The First Affiliated Hospital of Hebei University of Chinese Medicine， Shijiazhuang 050011，China
- Publication Type:Journal Article
- Keywords:
Xianglian Huazhuo prescription;
weighted gene co-expression network analysis （WGCNA）;
chronic atrophic gastritis;
proliferation;
cell cycle
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(8):128-136
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg-1， respectively）， and Morodan group （1.4 g·kg-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β1， Smad2 and Smad3 proteins， S/G2/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β1， suggesting the involvement of the TGF-β1 signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β1， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β1 and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β1/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.
