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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
OBJECTIVE: To observe the characteristics and regularity of the expression of bcl2 in intestine tissue of intestinal ischemia-reperfusion and its relationship with the occurrence of intestinal apoptosis. Methods: Sixteen Wistar rats were divided into normal control, mesenteric artery occlusion ischemia for 45 minutes, superior mesenteric artery occlusion for 45 minutes, reperfusion for 6 hours and reperfusion for 24 hours. Immunohistochemistry and terminal deoxyribo-transferase-mediated biotinylated deoxyuracil nick labeling (TUNEL technique) were used to observe the relationship between bcl2 gene expression and apoptosis in the above groups. Results: The superior mesenteric artery occlusion can lead to the increase of intestinal mucosal apoptosis and the activation of bcl2 gene expression. In the normal intestinal bcl2 expression was negative, ischemia can induce bcl2 expression, and in the bcl2 expression increased while apoptotic cells decreased. Compared with the 6-hour reperfusion group, the expression of bcl-2 in intestinal tissue 24 hours after reperfusion increased not only the intensity but also the features of extensive distribution and multiple tissues. Conclusion: The activation of bcl2 gene expression by ischemia-reperfusion is one of the most important anti-apoptotic mechanisms in vivo. Fibroblast growth factor reduces intestinal apoptosis may be related to its activation and up-regulated bcl2 gene expression