Department of Gastroenterology, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120, PR China; Guangzhou University of Chinese Medicine, Guangzhou 510405, PR China.
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, PR China.
Int Immunopharmacol. 2017 Nov;52:211-217. doi: 10.1016/j.intimp.2017.09.011. Epub 2017 Sep 21.
The present study aimed to investigate the potential protective effects of Astragaloside IV (AS-IV) against ethanol-induced gastric mucosal injury in rats. The animals were divided into 7 groups and pretreated with vehicle, various doses of AS-IV (1,2 and 4mg/kg, i.p.) or omeprazole (40mg/kg), 75min later, the gastric mucosal injury was induced by oral administration of ethanol. One hour after ethanol ingestion, the rats were euthanized and gastric tissues were collected to biochemical analyze. Myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), interleukin 10 (IL-10), nuclear factor kappa B (NF-κB) p65 protein, TNF receptor-associated factor 2 (TRAF2) and nuclear NF-κB (nNF-κB) proteins were estimated by enzyme-linked immunosorbent assay or western blot analysis. The gastric mucosal lesions were assessed by macroscopic and histopathological examinations. The results showed pretreatment with AS-IV attenuated the severity of ethanol gastric mucosal damage as evidenced by lowering of injury scores, histopathologic aberrations and leukocyte invasion. These actions were analogous to the reference omeprazole. AS-IV suppressed gastric inflammation by curbing of MPO, TNF-α levels along with NF-κB p65 and TRAF2 expression. It also augmented the anti-inflammatory IL-10 levels. Meanwhile, AS-IV could inhibit NF-κB transcription by inhibiting the expression of NF-κB p65 and increasing the expression of nNF-κB. It seems that AS-IV as an anti-inflammatory agent may have a protective effect against ethanol-induced mucosal injury by inhibition of neutrophil infiltration and reducing the expression of NF-κB p65, TRAF2 and inflammatory cytokines via regulating TNF-α/NF-κB signal pathway in gastric tissue.
本研究旨在探讨黄芪甲苷（AS-IV）对乙醇诱导的大鼠胃黏膜损伤的潜在保护作用。动物分为 7 组，分别给予 vehicle、不同剂量的 AS-IV（1、2 和 4mg/kg，ip）或奥美拉唑（40mg/kg）预处理，75min 后给予乙醇灌胃诱导胃黏膜损伤。乙醇摄入 1 小时后处死大鼠，收集胃组织进行生化分析。髓过氧化物酶（MPO）、肿瘤坏死因子-α（TNF-α）、白细胞介素 1β（IL-1β）、白细胞介素 10（IL-10）、核因子 kappa B（NF-κB）p65 蛋白、肿瘤坏死因子受体相关因子 2（TRAF2）和核 NF-κB（nNF-κB）蛋白通过酶联免疫吸附试验或 Western blot 分析进行估计。胃黏膜病变通过宏观和组织病理学检查进行评估。结果表明，AS-IV 预处理可减轻乙醇胃黏膜损伤的严重程度，表现为损伤评分降低、组织学异常和白细胞浸润减少。这些作用与参考奥美拉唑相似。AS-IV 通过抑制 MPO、TNF-α 水平以及 NF-κB p65 和 TRAF2 表达来抑制胃炎症。它还增加了抗炎性 IL-10 水平。同时，AS-IV 可通过抑制 NF-κB p65 的表达和增加 nNF-κB 的表达来抑制 NF-κB 转录。AS-IV 作为一种抗炎剂，可能通过抑制中性粒细胞浸润和减少 NF-κB p65、TRAF2 和炎症细胞因子的表达，通过调节 TNF-α/NF-κB 信号通路，对乙醇诱导的黏膜损伤具有保护作用。
