为太极凤目丸通过调节NF-κB通路来阻止与炎症相关的胃肠化生和畸形。
Wei-fu-chun tablet halted gastric intestinal metaplasia and dysplasia associated with inflammation by regulating the NF-κB pathway.
发表日期:2023 Aug 09
作者:
Dong Xie, Chao Wu, Dan Wang, Bahaji Azami Nisma Lena, Ningning Liu, Guan Ye, Mingyu Sun
来源:
JOURNAL OF ETHNOPHARMACOLOGY
摘要:
1982年,中国国家食品药品监督管理局批准的中药为复春片(WFC)已广泛应用于中国治疗多种慢性胃病,包括慢性萎缩性胃炎(CAG)和胃癌前病变。本研究旨在研究WFC治疗胃肠化生(GIM)和胃上皮内瘤变(GDys)的疗效和潜在机制。通过N-甲基-N'-硝基-N-亚硝基胍(MNNG)联合热敷、酒精损伤和间歇性禁食建立大鼠GIM和GDys模型,并进行WFC干预。检测体重、组织病理学、胃酸pH值、胃酸蛋白酶活性、胃肠化生指数和炎症。以WFC处理的大鼠骨髓源性巨噬细胞(BMDMs)受到LPS刺激。评估炎症因子和核因子-kappa B(NF-κB)信号通路。用WFC预处理的GES-1细胞受到MNNG和TNF-α刺激,检测胃肠化生指数、NF-κB信号通路和P65与CDX2之间的相互作用。WFC改善了大鼠GIM和GDys模型中的体重、组织病理学、胃酸pH值、胃蛋白酶活性、肠化生(CDX2)、炎症(IL-1β、IL-6和TNF-α)和胃粘膜巨噬细胞聚集(CD68)。WFC通过失活NF-κB信号通路抑制炎症(IL-1β和TNF-α)。WFC通过抑制CDX2启动子TSS上游区与P65的结合,降低CDX2的表达。WFC通过调节NF-κB信号通路来阻断与炎症相关的GIM和GDys。版权所有 © 2023 Elsevier B.V.发表。
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).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.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.WFC blocked GIM and GDys associated with inflammation by regulating the NF-κB pathway.Copyright © 2023. Published by Elsevier B.V.