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Endoplasmic reticulum stress response is involved in the pathogenesis of stress induced gastric lesions in rats

机译：内质网应激反应参与应激性胃病大鼠的发病机制

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摘要

Stress gastric ulcer is a serious complication, but the mechanism involved is not fully clarified. It is well known that mucosal cell apoptosis plays a crucial role in the pathogenesis of gastric ulceration. Recent studies have shown that endoplasmic reticulum (ER) stress is an important pathway leading to cellular apoptosis. To investigate the role of ER stress in the pathogenesis of stress gastric ulcer, we studied the alteration in the expression of ER stress markers GRP78 (glucose-regulated protein 78) and caspase-12 (an ER stress-specific proapoptotic molecule) and their relations with gastric mucosal apoptosis during development of stress gastric lesions in the water-immersion and restraint stress (WRS) model in rats. Rats developed severe gastric lesions after 6 h of WRS. Typical apoptosis was observed at the edge cells of WRS induced gastric lesions. Western blot analysis showed that GRP78 and activated caspase-12 were over-expressed in the gastric tissues of WRS rats. Immunchistochemical analysis demonstrated that increased GRP78 and caspase-12 were distributed only under the lesions. In addition, dithiothreitol and tunicamycin (ER stress inducers), which increased the expression of GRP78 and activated caspase-12, caused gastric mucosal injury and mucosal cell apoptosis in vitro. These findings suggest that ER stress might be involved in the development of stress gastric ulcer through an apoptotic mechanism. (c) 2006 Elsevier Inc. All rights reserved.
机译：应激性胃溃疡是一种严重的并发症，但其机制尚不完全清楚。众所周知，粘膜细胞凋亡在胃溃疡的发病机理中起着至关重要的作用。最近的研究表明，内质网应激是导致细胞凋亡的重要途径。为了研究内质网应激在应激性胃溃疡发病中的作用，我们研究了内质网应激标志物GRP78（葡萄糖调节蛋白78）和胱天蛋白酶12（内质网应激特异性凋亡分子）表达的变化及其关系。水浸和束缚应激（WRS）模型中应激性胃病变发展过程中胃黏膜细胞凋亡的变化WRS 6小时后，大鼠出现严重的胃部病变。在WRS诱导的胃部损伤的边缘细胞处观察到典型的凋亡。蛋白质印迹分析表明，WRS大鼠的胃组织中GRP78和活化的caspase-12过度表达。免疫组织化学分析表明，GRP78和caspase-12的增加仅分布在病变下。此外，二硫苏糖醇和衣霉素（ER应激诱导剂）增加了GRP78和活化的caspase-12的表达，在体外引起了胃黏膜损伤和黏膜细胞凋亡。这些发现表明内质网应激可能通过凋亡机制参与了应激性胃溃疡的发展。 （c）2006 Elsevier Inc.保留所有权利。

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