论文部分内容阅读
雄性Wistar大鼠30只,随机平均分为3组,正常对照组、糖尿病组、糖尿病甘草酸(30mg/kg/d)治疗组,腹腔注射链脲佐菌素(60mg/kg)诱发糖尿病。16周后,处死大鼠,分离肾脏,观察Bcl-2、Bax的表达,取部分肾皮质电镜病理观察。结果①糖尿病组肾脏Bcl-2蛋白表达减少、Bax蛋白表达增加,甘草酸治疗组的Bcl-2蛋白表达较糖尿病组增多,而Bax蛋白表达较糖尿病组减少,电镜观察糖尿病组呈明显细胞凋亡形态学改变,甘草酸治疗组减轻。②糖尿病肾小球基底膜增厚,系膜区域扩大,甘草酸治疗组病变减轻。结论①糖尿病血糖升高可能调节Bcl-2、Bax蛋白的表达诱导细胞凋亡,而参与DN的发生与发展。②甘草酸可调查Bax、Bcl-2的表达抑制细胞凋亡,明显改善糖尿病大鼠肾脏结构与功能,延缓DN的发展。
Thirty male Wistar rats were randomly divided into three groups randomly. The rats in normal control group, diabetes mellitus group and diabetic glycyrrhizin group (30mg / kg / d) were injected intraperitoneally with streptozotocin (60mg / kg) to induce diabetes mellitus. After 16 weeks, the rats were sacrificed, the kidneys were separated and the expressions of Bcl-2 and Bax were observed. The pathological changes of renal cortex were observed by electron microscopy. Results ① The expression of Bcl-2 protein and Bax protein were increased in the diabetic group. The expression of Bcl-2 protein in glycyrrhizinate group was higher than that in the diabetic group, while the expression of Bax protein was lower than that in the diabetic group. The apoptosis of the diabetic group was obvious Morphological changes, glycyrrhizinate treatment group reduced. ② diabetic glomerular basement membrane thickening, mesangial area expanded glycyrrhizinate treatment group lesion. Conclusions ① The hyperglycemia of diabetes may regulate the expression of Bcl-2 and Bax proteins and induce the apoptosis, which is involved in the occurrence and development of DN. Glycyrrhizin can be investigated Bax, Bcl-2 expression inhibition of apoptosis, significantly improve the diabetic rat kidney structure and function, delay the development of DN.