【摘要】 目的　探讨糖尿病大鼠冠状动脉内皮细胞(下称内皮细胞)凋亡的机制,以及凋亡与Fas基因、bcl-2基因表达之间的关系。　方法　实验大鼠分为未治疗组、胰岛素治疗组和正常对照组,每组8只,分别于第0周和第16周时处死检测一般指标,并观察内皮细胞的凋亡百分数(TUNEL法)、bcl-2基因、Fas基因的表达(免疫组化法)、内皮细胞超微结构的改变(电镜)。　结果　(1)16 周时,未治疗组比治疗组、正常对照组大鼠体重减轻,差异有统计学意义(P<0.05);血糖及糖化血红蛋白(HbA1c)显著高于后两组(P<0.05),内皮细胞凋亡数目明显增加,差异有统计学意义(P<0.05)。未治疗组Fas基因表达增加,而 bcl-2 基因表达降低,差异有统计学意义(P<0.01)。未治疗组可观察到较明显的内皮细胞凋亡的形态学改变。　结论　高血糖是实验大鼠内皮细胞凋亡强烈相关因素,凋亡的发生与Fas基因表达上调、bcl-2基因表达降低相关。更多还原

【Abstract】 Objective To explore the relationships between the hyperglycemia and apoptosis of coronary artery endothelial cells as well as expression of the apoptotic gene of diabetic rats. Methods The STZ-induced Wistar diabetic rats were divided into three groups: diabetic rats without （treatment;） the insulin-treated diabetic rats; and the control. At 0 and 16 weeks, the coronary artery outlets of the rats were collected as experimental material to examine apoptosis by using TUNEL, electromicroscopic changes and related gene expression with immunohistochemistry method. Meanwhile, the blood samples were collected to examine levels of TG,TC,HDL, LDL. Results The body weights were decreased in treated DM （205±23 vs 243±28 gram in control） and untreated DM （（169±25） vs 243±28 gram in control） （P<0.05）. HbA₁c levels were higher in treated MD （4.0±0.2% vs 3.4±0.3% in control） and untreated DM （8.2±0.4% vs 3.4±0.3% vs control） （P<0.05） significantly. The numbers of endothelial cell apoptosis were increased in untreated DM （22.8±6.9 vs 5.4±2.4% in control P<0.05） and in no significant change in treated DM （4.9±2.0% vs 5.4±2.4% in control, P>0.05）. Compared with control, the untreated DM had increased fas expression （62±12% vs 26±7%,P<0.05）, and decreased bcl-2 expression （18±5% vs 41±10%, P<0.05） while the treated DM had the same levels of fas and bcl-2 expression （28±8% vs 26±7% and 40±10% vs 41±10% separately, all P>0.05） as those of control. Conclusions Hyperglycemia is a apoptotic factor of vascular endothelial cell of diabetic rats; the apoptosis is correlated with up-regulation of expression of fas gene as well as down-regulation of expression of bcl-2 gene in diabetic rats.更多还原