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目的探讨血管紧张素Ⅱ受体拮抗剂伊贝沙坦对糖尿病大鼠心脏的保护作用及其一氧化氮(NO)机制。方法将30只Wistar大鼠随机分为对照组、糖尿病组和伊贝沙坦组3组,每组10只。大鼠腹腔一次注射2g/L链脲佐菌素(50mg/kg)造模,造模后12周终止实验处死大鼠,取血、尿和心脏标本,测定尿量、体质量、心脏质量/体质量的比值、血糖、糖化血红蛋白(HbA1c);测定血清和心脏组织NO的含量;并通过免疫组化观察心肌诱生型一氧化氮合酶(iNOS)的表达,RT-PCR检测iNOSmRNA的表达。结果12周终止实验时,糖尿病组和伊贝沙坦组大鼠的尿量、心脏质量/体质量比值、血糖、HbA1c、尿液、血清和心脏组织的NO水平均明显高于对照组,而体质量明显低于对照组(P<0.05);伊贝沙坦组大鼠的心脏质量/体质量比值、尿液、血清和心脏组织的NO水平明低于糖尿病组(P<0.05)。免疫组化发现伊贝沙坦组大鼠心脏组织的iNOS表达明显降低。RT-PCR发现伊贝沙坦组大鼠心脏组织的iNOSmRNA表达明显降低。结论NO和iNOS参加了糖尿病心肌病的发生,伊贝沙坦能抑制糖尿病大鼠心肌iNOS的基因和蛋白表达,减少NO产生。
Objective To investigate the protective effect of irbesartan, an angiotensin Ⅱ receptor antagonist, on the heart of diabetic rats and its mechanism of nitric oxide (NO). Methods Thirty Wistar rats were randomly divided into three groups: control group, diabetic group and irbesartan group, with 10 in each group. The rats were injected intraperitoneally with 2g / L streptozotocin (50mg / kg), and the rats were sacrificed 12 weeks after the model was established. The blood, urine and heart samples were taken and the urine volume, body weight and heart mass / (HbA1c). The content of nitric oxide (NO) in serum and heart tissue was measured. The expression of iNOS was detected by immunohistochemistry. The expression of iNOS mRNA was detected by RT-PCR. . Results At the end of 12 weeks, the urine volume, heart mass / body weight ratio, blood glucose, HbA1c, urine, serum and cardiac NO levels in diabetic group and irbesartan group were significantly higher than those in control group (P <0.05). The heart mass / body weight ratio, the level of NO in urine, serum and heart tissue in irbesartan group were significantly lower than those in diabetic group (P <0.05). Immunohistochemistry showed that the expression of iNOS in the heart tissue of irbesartan group was significantly decreased. RT-PCR showed that the expression of iNOS mRNA in the heart tissue of irbesartan group was significantly decreased. Conclusion NO and iNOS participate in the development of diabetic cardiomyopathy. Irbesartan can inhibit the gene and protein expression of iNOS in diabetic rats and decrease the production of NO.