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为探讨内皮素 (ET) 1在应激性溃疡 (SU)发病中的意义 ,以大鼠冷束缚应激溃疡 (CRS)为模型 ,采用免疫组化及放免方法 ,观察研究应激前后大鼠胃粘膜组织ET 1表达分布、含量及胃粘膜损伤溃疡指数 (UI)等变化情况。结果显示 ,ET 1阳性表达物质主要分布于胃粘膜血管内皮细胞、胃粘膜上皮细胞、粘膜肌层平滑肌细胞的胞浆 ,应激 3h后胃粘膜组织ET 1阳性表达细胞数量与强度均较正常对照组明显增加(P <0 0 5 )。放免显示应激 1h后胃粘膜组织ET 1含量即较正常对照组明显升高 (P <0 0 1) ,且在应激后 12h内呈持续升高状态 ,同时随着ET 1的升高 ,UI不断增加 ,两者呈显著正相关 (r=0 98,P <0 0 1)。提示在冷束缚应激诱导大鼠SU形成过程中 ,胃粘膜组织局部可大量增加ET 1的合成、分泌 ,从而参与SU的病理生理过程 ,可能是胃粘膜损伤的重要致病因子。
To investigate the significance of endothelin (ET) 1 in the pathogenesis of stress ulcer (SU), the model of cold restraint stress ulcer (CRS) was used in rats. Immunohistochemistry and radioimmunoassay were used to observe the effects of endothelin (ET) The distribution and content of ET 1 in gastric mucosa and the content of gastric mucosal injury and ulcer index (UI). The results showed that the expression of ET 1 was mainly distributed in the cytoplasm of gastric mucosal vascular endothelial cells, gastric mucosal epithelial cells and mucosal smooth muscle cells. The number and intensity of ET 1 positive cells in gastric mucosa after 3 h of stress were higher than those in normal controls Group increased significantly (P <0 05). Radioimmunoassay showed that the content of ET 1 in gastric mucosa was significantly higher than that in normal control group (P <0.01) after 1 h of stress, and continued to increase within 12 h after stress. With the increase of ET 1, There was a significant positive correlation between UI and UI (r = 0 98, P <0.01). It is suggested that during the process of cold restraint stress-induced rat SU formation, local synthesis and secretion of ET 1 may be greatly increased in gastric mucosa tissues, which may participate in the pathophysiology of SU and may be an important causative factor of gastric mucosal injury.