缺血-再灌注诱导bcl2基因表达及其对肠道细胞凋亡的影响

目的：观察缺血再灌注肠道组织原癌基因ｂｃｌ２表达的特征、规律以及与肠道细胞凋亡发生的关系。方法：将１６只Ｗｉｓｔａｒ大鼠分成正常对照、肠系膜上动脉夹闭缺血４５分钟、肠系膜上动脉夹闭４５分钟与再灌注６小时和再灌注２４小时４组。用免疫组化法和末端脱氧核糖转移酶介导的生物素化脱氧尿嘧啶缺刻标记技术（ＴＵＮＥＬ技术）分别观察以上各组肠道组织细胞ｂｃｌ２基因表达与凋亡发生的关系。结果：肠系膜上动脉夹闭可以导致肠粘膜细胞凋亡发生增加与激活ｂｃｌ２基因表达。在正常肠道ｂｃｌ２表达为阴性，缺血可诱导ｂｃｌ２表达，并且在ｂｃｌ２表达增加的同时凋亡细胞逐渐减少。与再灌注６小时组相比，再灌注２４小时肠道组织ｂｃｌ２表达不仅强度明显增加，而且还有分布广泛与涉及多种组织的特点。结论：缺血再灌注激活ｂｃｌ２基因表达是体内最重要的抗凋亡机制之一。成纤维细胞生长因子减轻肠道凋亡现象可能与其激活和上调ｂｃｌ２基因表达有关

Bcl2 gene expression and its effect on apopto sis in intestine after ischemiareperfusion in rats

Objective:To investigate the characteristic of bcl2 gene expression in intestine after ischemiareperfusion injury,and its possible role in regulating apoptosis in intestine.Methods:Wistar rats were subjected to superior mesenteric artery occlusion (45 minutes) followed by reperfusion (6 hours and 24 hours).16 rats were divided into four groups as follows:normal,ischemia (45 minutes),ischemia (45 minutes) plus reperfusion (6 hours) and ischemia (45 minutes) plus reperfusion (24 hours).After being scarified on schedule,the biopsies of small intestines were harvested for bcl2 gene expression analysis by immunohistochemical method or apoptosis detection by terminal deoxynucleotidy transferase mediated dUTPbiotin nickend labeling(TUNEL) technique.Results:In normal intestine,bcl2 gene expression could not be detected.After ischemia insult,bcl2 gene was expressed in intestine,but the expression signal was only localized mucosa.At 6 and 24 hours after reperfusion,the bcl2 gene expression was increased significantly compared with the ischemia group.The changes in apoptosis were quite different from bcl2 gene expression,the apoptosis signal was reduced,while bcl2 gene was markedly expressed.Conclusions:Our results indicate that the bcl2 gene expression in intestine after ischemiareperfusion insult play an important role in regulating apoptosis,it suggests that the effect of fibroblast growth factor on intestine repair may associated with upregulated bcl2 gene expression.