Department of General Surgery, School of Medicine, South China University of Technology, Guangzhou 510006, China; Department of General Surgery, The Sixth Medical Center of Chinese PLA General Hospital, Beijing 100048, China.
Department of General Surgery, The First Medical Center of Chinese, PLA General Hospital, Beijing 100853, China.
Int Immunopharmacol. 2022 Oct;111:109122. doi: 10.1016/j.intimp.2022.109122. Epub 2022 Aug 11.
As a common disease of the digestive system, chronic gastritis is inflammation of the gastric mucosa caused by various factors. Helicobacter pylori (H. pylori) is one of the main causes of chronic gastritis, which can lead to gastric mucosal damage and gland atrophy, thereby promoting gastrocarcinogenesis. Oxidative stress and the inflammatory response are important mechanisms of H. pylori-induced gastritis. 6'-O-Galloylpaeoniflorin (GPF) is a substance isolated from peony root with antioxidant and anti-inflammatory activities. However, its role and mechanism in the pathogenesis of H. pylori-induced chronic gastritis remain unclear. This study explored the effects of GPF on H. pylori-induced gastric mucosal oxidative stress and inflammation using flow cytometry, western blotting, real-time quantitative PCR, and immunohistochemistry. We found that H. pylori infection increased oxidative stress and expression of inflammatory cytokines in vitro and in vivo and that these outcomes were inhibited by GPF. Furthermore, GPF activated nuclear factor erythroid-related factor-2 (Nrf2) and its downstream target genes in H. pylori-infected GES-1 cells and mice. The anti-inflammatory and antioxidant effects of GPF on H. pylori-infected cells were attenuated by an Nrf2 inhibitor. Taken together, these data suggest that GPF reduces H. pylori-induced gastric mucosa injury by activating Nrf2 signaling and that GPF is a potential candidate for the treatment of H. pylori-associated gastritis.
作为一种常见的消化系统疾病，慢性胃炎是由多种因素引起的胃黏膜炎症。幽门螺杆菌（H. pylori）是慢性胃炎的主要原因之一，它可导致胃黏膜损伤和腺体萎缩，从而促进胃癌变。氧化应激和炎症反应是 H. pylori 引起的胃炎的重要机制。6'-O-没食子酰基芍药苷（GPF）是从牡丹根中分离得到的一种具有抗氧化和抗炎活性的物质。然而，其在 H. pylori 诱导的慢性 gastritis 发病机制中的作用和机制尚不清楚。本研究采用流式细胞术、Western blot、实时定量 PCR 和免疫组织化学方法探讨了 GPF 对 H. pylori 诱导的胃黏膜氧化应激和炎症的影响。我们发现 H. pylori 感染在体外和体内均可增加氧化应激和炎症细胞因子的表达，而 GPF 可抑制这些结果。此外，GPF 在 H. pylori 感染的 GES-1 细胞和小鼠中激活了核因子红细胞相关因子-2（Nrf2）及其下游靶基因。Nrf2 抑制剂可减弱 GPF 对 H. pylori 感染细胞的抗炎和抗氧化作用。综上所述，这些数据表明 GPF 通过激活 Nrf2 信号通路减轻 H. pylori 诱导的胃黏膜损伤，GPF 是治疗 H. pylori 相关性 gastritis 的潜在候选药物。
