胃复春片通过调控 NF-κB 通路抑制炎症相关的胃黏膜肠上皮化生及异型增生。
Wei-fu-chun tablet halted gastric intestinal metaplasia and dysplasia associated with inflammation by regulating the NF-κB pathway.
机构信息
Shuguang Hospital, Key Laboratory of Liver and Kidney Diseases (Ministry of Education), Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China; Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Department of Oncology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
出版信息
J Ethnopharmacol. 2024 Jan 10;318(Pt B):117020. doi: 10.1016/j.jep.2023.117020. Epub 2023 Aug 9.
ETHNOPHARMACOLOGICAL RELEVANCE
Chi006Eese herbal medicine Weifuchun Tablets (WFC) approved by the State Food and Drug Administration in 1982 has been widely used in treating a variety of chronic stomach disorders including Chronic atrophic gastritis (CAG) and Gastric precancerous lesions in China clinically. This study aimed to investigate the efficacy and potential mechanism of WFC in treating Gastric intestinal metaplasia (GIM) and Gastric dysplasia (GDys).
MATERIALS AND METHODS
Rat GIM and GDys established by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) combined with hot paste, ethanol injury, and intermittent fasting were intervened by WFC. Body weight, histopathology, pH of gastric acid, pepsin activity, intestinal metaplasia index and inflammation were detected. Rat bone marrow derived macrophages (BMDMs) pretreated with WFC were stimulated by LPS. Inflammatory factors and the nuclear factor-kappa B (NF-κB) pathway were assessed. GES-1 cells pretreated by WFC were stimulated by MNNG and TNF-α, intestinal metaplasia index, the NF-κB pathway and interaction between P65 and CDX2 were detected.
RESULTS
WFC improved rat body weight, histopathology, pH value of gastric acid, activity of gastric pepsin, intestinal metaplasia (CDX2), inflammation (IL-1β, IL-6 and TNF-α), macrophage aggregation (CD68) in gastric mucosa in rat GIM and GDys. WFC inhibited inflammation (IL-1β and TNF-α) by inactivating the NF-κB pathway. WFC reduced the expression of CDX2 by inhibiting the binding of CDX2 promoter TSS upstream region with p65.
CONCLUSION
WFC blocked GIM and GDys associated with inflammation by regulating the NF-κB pathway.
民族药理学相关性
1982 年，国家食品药品监督管理局批准的中草药胃复春片（WFC）已在中国临床上广泛用于治疗各种慢性胃病，包括慢性萎缩性胃炎（CAG）和胃癌前病变。本研究旨在探讨 WFC 治疗胃黏膜肠上皮化生（GIM）和胃发育不良（GDys）的疗效及其潜在机制。
材料与方法
采用 N-甲基-N'-硝基-N-亚硝基胍（MNNG）联合热糊、乙醇损伤和间歇性禁食建立大鼠 GIM 和 GDys 模型，用 WFC 干预。检测体重、组织病理学、胃酸 pH 值、胃蛋白酶活性、肠上皮化生指数和炎症。用 WFC 预处理大鼠骨髓来源巨噬细胞（BMDMs），用 LPS 刺激。评估炎症因子和核因子-κB（NF-κB）通路。用 WFC 预处理 GES-1 细胞，用 MNNG 和 TNF-α刺激，检测肠上皮化生指数、NF-κB 通路及 P65 与 CDX2 的相互作用。
结果
WFC 改善了大鼠 GIM 和 GDys 体重、组织病理学、胃酸 pH 值、胃蛋白酶活性、肠上皮化生（CDX2）、炎症（IL-1β、IL-6 和 TNF-α）、胃黏膜巨噬细胞聚集（CD68）。WFC 通过抑制 NF-κB 通路抑制炎症（IL-1β 和 TNF-α）。WFC 通过抑制 CDX2 启动子 TSS 上游区域与 p65 的结合，减少 CDX2 的表达。
结论
WFC 通过调节 NF-κB 通路阻断与炎症相关的 GIM 和 GDys。
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