Naito Yuji, Yoshikawa Toshikazu
Department of Medical Proteomics, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Redox Rep. 2006;11(6):243-53. doi: 10.1179/135100006X155021.
It has been proposed that neutrophil- and oxygen radical-dependent microvascular injuries are important prime events that lead to gastric mucosal injury induced by indomethacin. Reactive oxygen species (ROS) produced by activated neutrophils after indomethacin treatment cause gastric mucosal injury via ROS-mediated oxidation of important biomolecules such as lipid, protein, and DNA. In addition, it has been revealed that indomethacin-induced gastric mucosal injury occurs via gastric epithelial cell apoptosis. However, there is little known about the mechanism of indomethacin-triggered cellular response and apoptotic signaling in gastric mucosal cells. In the present study, we summarize the evidence that supports the involvement of oxidative stress and apoptosis in indomethacin-induced gastropathy, and review the gene expression profiles of gastric epithelial cells after indomethacin treatment determined by DNA microarray analysis.
有人提出，中性粒细胞和氧自由基依赖性微血管损伤是导致吲哚美辛诱导胃黏膜损伤的重要起始事件。吲哚美辛治疗后活化的中性粒细胞产生的活性氧（ROS）通过ROS介导的脂质、蛋白质和DNA等重要生物分子的氧化作用导致胃黏膜损伤。此外，已揭示吲哚美辛诱导的胃黏膜损伤通过胃上皮细胞凋亡发生。然而，关于吲哚美辛触发胃黏膜细胞的细胞反应和凋亡信号传导的机制知之甚少。在本研究中，我们总结了支持氧化应激和凋亡参与吲哚美辛诱导的胃病的证据，并回顾了通过DNA微阵列分析确定的吲哚美辛治疗后胃上皮细胞的基因表达谱。
