American journal of translational research · 2026
Jiangfu Fuwei granules alleviate chronic atrophic gastritis by suppressing angiogenesis through the PI3K-AKT-HIF1α pathway.
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Bi Yuqing, Chen Yanchun, Jiang Jimei, Mao Wangqi, Zhang Xiao, Liu Jiayi, Zhao Xin, Dong Yueqiu, Cai Yueqing, Li Mei, Li Xiang, Luan Yunpeng, Jiang Liyun
Аннотация
OBJECTIVE: Jiangfu Fuwei granules (JFFW) are a widely used clinical prescription for the treatment of chronic atrophic gastritis (CAG), but the underlying molecular mechanism remains to be explored. This study aimed to elucidate the therapeutic mechanism of JFFW in alleviating CAG.
METHODS: A CAG mouse model was established using a combined approach, and the mice were treated with JFFW for six weeks. Network pharmacology was used to screen for active ingredients and signaling pathways. Subsequently, in vivo experiments were conducted to verify the predicted mechanisms, including histologic evaluation, enzyme-linked immunosorbent assay, and immunohistochemical analysis. Furthermore, molecular docking was used to simulate the interaction between key active compounds and core protein targets.
RESULTS: In vivo experimental results demonstrated that JFFW effectively reversed gastric mucosal thinning and glandular loss in CAG mice. This treatment significantly restored serum pepsinogen levels and downregulated the expression of inflammatory cytokines, specifically interleukin-6, interleukin-1β, and tumor necrosis factor-α. Network pharmacology analysis identified 224 bioactive compounds and predicted the phosphoinositol 3-kinase (PI3K)-protein kinase B (AKT)-hypoxia-inducible factor 1-α (HIF1α) signaling pathway as a key target. Immunohistochemical results confirmed that JFFW treatment significantly inhibited the protein expression of phosphorylated AKT and HIF1α. Furthermore, reduced CD31 staining occurred consistent with a decrease in microvessel density. Molecular docking analysis further confirmed that the main components of JFFW had a good binding affinity to PI3K protein.
CONCLUSION: The therapeutic effect of JFFW on CAG is mainly achieved by inhibiting the PI3K-AKT-HIF1α signaling pathway, thereby suppressing abnormal angiogenesis and gastric inflammation.
METHODS: A CAG mouse model was established using a combined approach, and the mice were treated with JFFW for six weeks. Network pharmacology was used to screen for active ingredients and signaling pathways. Subsequently, in vivo experiments were conducted to verify the predicted mechanisms, including histologic evaluation, enzyme-linked immunosorbent assay, and immunohistochemical analysis. Furthermore, molecular docking was used to simulate the interaction between key active compounds and core protein targets.
RESULTS: In vivo experimental results demonstrated that JFFW effectively reversed gastric mucosal thinning and glandular loss in CAG mice. This treatment significantly restored serum pepsinogen levels and downregulated the expression of inflammatory cytokines, specifically interleukin-6, interleukin-1β, and tumor necrosis factor-α. Network pharmacology analysis identified 224 bioactive compounds and predicted the phosphoinositol 3-kinase (PI3K)-protein kinase B (AKT)-hypoxia-inducible factor 1-α (HIF1α) signaling pathway as a key target. Immunohistochemical results confirmed that JFFW treatment significantly inhibited the protein expression of phosphorylated AKT and HIF1α. Furthermore, reduced CD31 staining occurred consistent with a decrease in microvessel density. Molecular docking analysis further confirmed that the main components of JFFW had a good binding affinity to PI3K protein.
CONCLUSION: The therapeutic effect of JFFW on CAG is mainly achieved by inhibiting the PI3K-AKT-HIF1α signaling pathway, thereby suppressing abnormal angiogenesis and gastric inflammation.