NSAIDs and Acidic Environment Induce Gastric Mucosal Cellular Mitochondrial Dysfunction
NSAIDs and Acidic Environment Induce Gastric Mucosal Cellular Mitochondrial Dysfunction
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DOI：
10.1159/000334685
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发表时间：
2012-01-01
期刊：
影响因子：
3.2
通讯作者：
Hyodo, Ichinosuke
中科院分区：
文献类型：
--
作者：
Nagano, Yumiko;Matsui, Hirofumi;Hyodo, Ichinosuke
非甾体类抗炎药（NSAID）常引起胃肠道并发症，如胃溃疡和糜烂。最近关于发病机制的研究表明，NSAID通过在线粒体中产生超氧化物诱导胃上皮细胞的脂质过氧化，独立于环氧合酶抑制和随后的前列腺素缺乏。近年来，胃内盐酸（HCI）被认为是胃粘膜损伤的一个诱发因素，并据报道在体外诱导细胞脂质过氧化。我们假设胃酸和NSAID治疗协同诱导胃上皮细胞的细胞损伤。我们用酸性溶液和NSAID处理胃上皮RGM1细胞，检测细胞损伤、脂质过氧化、线粒体跨膜电位和线粒体超氧化物。我们用酸性溶液预处理RGM1细胞0.5小时，然后用每种NSAID处理15小时，发现暴露于酸和NSAID确实诱导细胞损伤。我们假设胃酸和NSAID治疗协同诱导线粒体超氧化物产生，从而诱导胃细胞损伤。版权所有（C）2012 S. Karger AG，巴塞尔
Non-steroidal anti-inflammatory drugs (NSAIDs) often cause gastrointestinal complications such as gastric ulcers and erosions. Recent studies on the pathogenesis have revealed that NSAIDs induce lipid peroxidation in gastric epithelial cells by generating superoxide in mitochondria, independently with cyclooxygenase inhibition and the subsequent prostaglandin deficiency. More recently, gastric hydrochloric acid (HCI) has been regarded as an inciting factor of gastric mucosal injuries, and reportedly induced cellular lipid peroxidation in vitro. We hypothesized that gastric acid and NSAID treatment synergistically induce cellular injury in gastric epithelial cells. We treated gastric epithelial RGM1 cells with acidic solutions and NSAIDs, and examined cellular injury, lipid peroxidation, mitochondrial transmenbrane potential and mitochondrial superoxide. We pretreated RGM1 cells with the acidic solutions for 0.5 h and after that treated them with each NSAID for 15 h and found that the exposure to acid and NSAIDs indeed induced cellular injury. We hypothesized that gastric acid and NSAID treatment synergistically induce mitochondrial superoxide production, which induces gastric cellular injury. Copyright (C) 2012 S. Karger AG, Basel