内皮祖细胞对糖尿病心肌病大鼠氧化应激作用的研究

目的研究内皮祖细胞(Endothelial progenitor cells,EPCs)对链脲佐菌素诱导的糖尿病心肌病大鼠的氧化应激作用。方法通过腹腔注射链脲佐素诱导大鼠糖尿病心脏病模型,治疗组给予EPCs进行治疗。HE染色观察各组心肌组织的形态学改变;葡萄糖氧化酶法进行空腹血糖测定;检测各组大鼠血清中GSH和MDA含量;采用RT-PCR和Western blot方法检测大鼠心肌组织中iNOS和eNOS的表达水平。结果与正常对照组比较,糖尿病心肌病模型组心肌肥大,组织排列紊乱;血清GSH含量显著下降(P<0.01),MDA含量显著升高(P<0.01),心肌组织中iNOS和eNOSmRNA及蛋白的表达均显著升高(P<0.05)。经EPCs治疗后,GSH含量显著升高(P<0.01),MDA、iNOS和eNOS水平显著降低(P<0.05);心肌病理损伤得到修复。结论 EPCs可缓解由链脲佐菌素诱导的糖尿病心肌病,其作用机制可能与减少氧化应激、降低NOS水平有关。

Role of Endothelial Progenitor Cells in Diabetic Cardiomyopathy Rats with Oxidative Stress

Objective To study the role of endothelial progenitor cells （Endothelial progenitor cells, EPCs） in streptozotocin induced diabetic cardiomyopathy oxidative stress. Methods Diabetic rat model was induced by intraperitoneal injection of streptozotocin, treatment group was treated with intravenous injection of EPCs cells. Myocardial tissue morphological changes was detected by HE staining. Fasting blood glucose was detected by glucose oxidase method. The content of GSH and MDA in rat serum were detected by kit. The expression level of eNOS and iNOS of myocardial tissue in rats was measured by RT-PCR and Western blot. Results Compared with the control group, myocardial hypertrophy and tissue disorganization were observed in model group. The content of GSH in serum decreased and the content of MDA increased, iNOS in myocardial tissue and eNOS expression also increased. With the treatment of EPCs, the content of GSH picked up somewhat, while MDA, iNOS and eNOS levels dropped, at the same time, myocardial injury was improved. Conclusion EPCs can alleviate streptozotocin induced diabetic cardiomyopathy and its mechanism may be associated with a reduction in oxidative stress and NOS level.