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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。
Objective To investigate the oxidative stress effects of endothelial progenitor cells (EPCs) on diabetic rats with streptozotocin-induced diabetic cardiomyopathy. Methods The model of diabetic heart disease was induced by intraperitoneal injection of streptozotocin. EPCs were treated in the treatment group. The morphological changes of myocardium in each group were observed by HE staining; the fasting blood glucose was measured by glucose oxidase method; the contents of GSH and MDA in serum of rats in each group were detected; the expressions of iNOS and eNOS in myocardium were detected by RT-PCR and Western blot; The level of expression. Results Compared with the normal control group, cardiac hypertrophy and disordered organization of myocardium in diabetic cardiomyopathy model group were observed. Serum GSH level was significantly decreased (P <0.01), MDA content was significantly increased (P <0.01), myocardial tissue iNOS and eNOS mRNA and protein The expression was significantly increased (P <0.05). After EPCs treatment, the content of GSH was significantly increased (P <0.01), while the levels of MDA, iNOS and eNOS were significantly decreased (P <0.05). The pathological changes of myocardium were repaired. Conclusions EPCs can relieve diabetic cardiomyopathy induced by streptozotocin. Its mechanism may be related to reducing oxidative stress and decreasing NOS level.