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目的:探讨糖尿病骨骼肌凋亡相关蛋白Bcl-2和Bax表达的变化及意义。方法:选用Wistar大鼠24只,随机分成正常对照组、单纯缺血组、糖尿病组和糖尿病缺血组,每组6只。以四氧嘧啶50mg/kg尾静脉注射制造糖尿病模型。造模后2周结扎右股动脉制造缺血模型。10周后,以免疫组化方法观察腓肠肌中凋亡相关蛋白Bcl-2及Bax表达情况。结果:糖尿病组骨骼肌表现为普遍性萎缩,肌纤维变性坏死。与对照组比较糖尿病可使骨骼肌凋亡相关蛋白Bcl-2表达降低(P<0.05),Bax表达增高(P<0.05)。缺血可使骨骼肌Bax蛋白表达增高(P<0.05),但对Bcl-2表达的影响与对照组比较差异无统计学意义(P>0.05)。糖尿病与缺血对骨骼肌Bcl-2和Bax蛋白表达的影响无交互作用(P>0.05)。结论:糖尿病骨骼肌病变可能与Bcl-2与Bax蛋白比例下降促进细胞凋亡有关。
Objective: To investigate the changes and significance of Bcl-2 and Bax in skeletal muscle of diabetic patients. Methods: Twenty-four Wistar rats were randomly divided into normal control group, ischemia group, diabetic group and diabetic ischemia group, with 6 rats in each group. Alloxan 50mg / kg tail vein injection to create diabetes model. Ligation of the right femoral artery 2 weeks after modeling to create an ischemic model. After 10 weeks, the expression of Bcl-2 and Bax in gastrocnemius muscle was observed by immunohistochemistry. Results: The skeletal muscle of diabetic group showed general atrophy and myofibrosis. Compared with the control group, diabetes could decrease the expression of Bcl-2 and Bax in skeletal muscle (P <0.05). Ischemia can increase skeletal muscle Bax protein expression (P <0.05), but the impact of Bcl-2 expression compared with the control group was no significant difference (P> 0.05). The effects of diabetes mellitus and ischemia on the expression of Bcl-2 and Bax in skeletal muscle had no interaction (P> 0.05). Conclusion: Diabetic skeletal muscle lesions may be related to the decrease of Bcl-2 and Bax protein and apoptosis.