Microbial pathogenesis · 2026
Meihuacao extract in eradicating H.pylori: Network pharmacology analyses and experiment validation.
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Wang Ruijun, Li Huifang, Ge Rile, Pan Yuanming, He Zhanbiao
Аннотация
PURPOSE: This study aimed to investigate the intervention of Parnassia palustris Linn (Meihuacao, MHC) extract against Helicobacter pylori (H. pylori) using network pharmacology analysis and experimental validation.
METHODS: An active compound-target-disease network was constructed using network pharmacology and molecular docking. Mice were divided into normal, Hp, triple therapy, quadruple therapy, MHC, triple + MHC, and quadruple + MHC groups. The minimum inhibitory concentration (MIC) of MHC against the H. pylori SS1 standard strain was determined by agar dilution. The expression of BabA, CagA, and VacA were measured using real-time PCR. Animal experiments were performed to assess the Hp eradication rate. The levels of serum IL-2, CXCL2, and TNF-α were measured by ELISA. The expression of IL-2, cleaved caspase-3, CXCL2, HIF-1α, and PPAR-α in gastric tissue was detected by immunohistochemistry (IHC). Hp infection rate was determined using a rapid urease test. The stomach was observed by hematoxylin and eosin (HE) staining and transmission electron microscopy (TEM).
RESULTS: Interacted with core genes such as TNF, IL-2, and CXCL2 (the murine functional analog of human IL-8). KEGG pathway analysis indicated that these core genes were involved in the PI3K/Akt, TNF and HIF-1 signaling pathways. In the MHC group, the expression of BabA, CagA, and VacA was decreased, and gastric mucosal hemorrhage and ulceration were improved, with reduced H. pylori infection compared with the Hp group. The H. pylori eradication rates in the triple + MHC or quadruple + MHC groups were increased, accompanied by intact mitochondria and microvilli. IL-2 levels were increased in the other groups, while CXCL2 and TNF-α levels were reduced. IHC results were consistent with the analysis of network pharmacology.
CONCLUSIONS: MHC effectively eradicates Hp and protects gastric mucosa, suggesting its potential for clinical application.
METHODS: An active compound-target-disease network was constructed using network pharmacology and molecular docking. Mice were divided into normal, Hp, triple therapy, quadruple therapy, MHC, triple + MHC, and quadruple + MHC groups. The minimum inhibitory concentration (MIC) of MHC against the H. pylori SS1 standard strain was determined by agar dilution. The expression of BabA, CagA, and VacA were measured using real-time PCR. Animal experiments were performed to assess the Hp eradication rate. The levels of serum IL-2, CXCL2, and TNF-α were measured by ELISA. The expression of IL-2, cleaved caspase-3, CXCL2, HIF-1α, and PPAR-α in gastric tissue was detected by immunohistochemistry (IHC). Hp infection rate was determined using a rapid urease test. The stomach was observed by hematoxylin and eosin (HE) staining and transmission electron microscopy (TEM).
RESULTS: Interacted with core genes such as TNF, IL-2, and CXCL2 (the murine functional analog of human IL-8). KEGG pathway analysis indicated that these core genes were involved in the PI3K/Akt, TNF and HIF-1 signaling pathways. In the MHC group, the expression of BabA, CagA, and VacA was decreased, and gastric mucosal hemorrhage and ulceration were improved, with reduced H. pylori infection compared with the Hp group. The H. pylori eradication rates in the triple + MHC or quadruple + MHC groups were increased, accompanied by intact mitochondria and microvilli. IL-2 levels were increased in the other groups, while CXCL2 and TNF-α levels were reduced. IHC results were consistent with the analysis of network pharmacology.
CONCLUSIONS: MHC effectively eradicates Hp and protects gastric mucosa, suggesting its potential for clinical application.