Shian W M, Sasaki I, Kamiyama Y, Naito H, Matsuno S, Miyazawa T
First Department of Surgery, School of Medicine, Tohoku University, Sendai, Japan.
Surg Today. 2000;30(1):49-53. doi: 10.1007/PL00010046.
This study was designed to determine the effect of water-immersion-restraint stress (WIRS) and pretreatment by reduced glutathione on both the production of gastric mucosal lesions and the content of gastric mucosal phosphatidylcholine hydroperoxide (PCOOH). Sprague-Dawley rats were divided into control and treatment groups (treated with reduced glutathione before stress). After graded durations of WIRS, the macroscopic ulcer index (UI) was measured and the PCOOH content was examined by a chemiluminescence-high performance liquid chromatography assay. The UI in the control group increased significantly in a time-dependent fashion. Elevation of the PCOOH level was observed in combination with the UI for up to 2h of WIRS, but then showed a declining tendency. Pretreatment with reduced glutathione significantly lowered both the UI and the PCOOH level. Lipid peroxidation is probably involved in the pathogenesis of gastric injury induced by WIRS at least in the early phases. However, in the late phases, other mechanisms causing gastric mucosal lesions may also be involved. We therefore believe this study to be the first to accurately and quantitatively assess the degree of lipid peroxidation in the gastric mucosa as a result of stress.
本研究旨在确定水浸束缚应激(WIRS)及还原型谷胱甘肽预处理对胃黏膜损伤的产生以及胃黏膜磷脂酰胆碱氢过氧化物(PCOOH)含量的影响。将Sprague-Dawley大鼠分为对照组和治疗组(应激前用还原型谷胱甘肽处理)。在不同时长的WIRS后,测量宏观溃疡指数(UI),并通过化学发光-高效液相色谱法检测PCOOH含量。对照组的UI呈时间依赖性显著增加。在长达2小时的WIRS过程中,PCOOH水平升高并与UI升高同时出现,但随后呈下降趋势。还原型谷胱甘肽预处理显著降低了UI和PCOOH水平。脂质过氧化可能至少在早期阶段参与了WIRS诱导的胃损伤的发病机制。然而,在后期阶段,可能还涉及导致胃黏膜损伤的其他机制。因此,我们认为本研究首次准确且定量地评估了应激导致的胃黏膜脂质过氧化程度。