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L-抗坏血酸-2-葡萄糖苷通过线粒体途径抑制幽门螺杆菌诱导的胃上皮细胞凋亡。

L-ascorbic Acid-2-Glucoside inhibits Helicobacter pylori-induced apoptosis through mitochondrial pathway in Gastric Epithelial cells.

机构信息

Department of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, China.

Department of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, China.

出版信息

Biomed Pharmacother. 2018 Jan;97:75-81. doi: 10.1016/j.biopha.2017.10.030. Epub 2017 Nov 6.

DOI:10.1016/j.biopha.2017.10.030
PMID:29080461
Abstract

Helicobacter pylori (H. pylori) infection is the major cause for gastritis, peptic ulcer, and gastric cancer. Elevated oxidative stress, mitochondrial dysfunction and apoptotic death of gastric epithelial cells are typical hallmarks of H. pylori infection. Ascorbic Acid 2-Glucoside (AA2G) is a stable version of Vitamin C, that binds glucose to conventional vitamin C. AA2G has free radical scavenging activities and anti-apoptotic abilities. However, the protective effect of AA2G against H. pylori-infection in gastric epithelial cells is yet unknown. In this study, we investigated the effects of AA2G in human H. pylori-infected gastric epithelial cells. AA2G could remarkably ameliorate H. pylori-induced oxidative stress, including the levels of intracellular reactive oxygen species (ROS) and 4-hydroxynonenal (4-HNE). Importantly, AA2G treatment also improved mitochondrial function by restoring the level of ATP and mitochondrial membrane potential (MMP). Furthermore, AA2G reduced apoptosis induced by H. pylori through modulation of mitochondria-dependent apoptotic pathways. Our findings suggest that AA2G has a protective effect against H. pylori infection in gastric epithelial cells.

摘要

幽门螺杆菌(H. pylori)感染是胃炎、消化性溃疡和胃癌的主要原因。氧化应激升高、线粒体功能障碍和胃上皮细胞凋亡是 H. pylori 感染的典型特征。抗坏血酸 2-葡萄糖苷(AA2G)是维生素 C 的稳定形式,它将葡萄糖与常规维生素 C 结合。AA2G 具有自由基清除活性和抗凋亡能力。然而,AA2G 对胃上皮细胞中 H. pylori 感染的保护作用尚不清楚。在这项研究中,我们研究了 AA2G 对人 H. pylori 感染胃上皮细胞的影响。AA2G 可显著改善 H. pylori 诱导的氧化应激,包括细胞内活性氧(ROS)和 4-羟基壬烯醛(4-HNE)的水平。重要的是,AA2G 通过恢复 ATP 和线粒体膜电位(MMP)水平来改善线粒体功能。此外,AA2G 通过调节线粒体依赖性凋亡途径减少 H. pylori 诱导的细胞凋亡。我们的研究结果表明,AA2G 对胃上皮细胞中 H. pylori 感染具有保护作用。

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