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目的研究2型糖尿病(T2DM)大鼠心肌氧化应激与抗氧化能力在心肌损伤发病机制中的作用,为治疗T2DM并发症提供科学依据。方法 SD大鼠32只,随机分为4组,对照组8周组和12周组,糖尿病组8周组和12周组,每组8只。对照组正常饲料喂养,链脲佐菌素(STZ)50 mg/kg诱发T2DM大鼠模型。采用硝酸还原酶法测定心肌一氧化氮(NO)含量,化学比色法测定一氧化氮合酶(NOS)活力、丙二醛(MDA)含量以及超氧化物歧化酶(SOD)活力。结果糖尿病组第8周、第12周NO、MDA含量,NOS活力均升高,SOD活力降低,差异均有统计学意义(P<0.05,P<0.01)。结论 T2DM大鼠随着病程延长,心肌抗氧化能力逐步下降,导致心肌氧化应激损伤。
Objective To investigate the role of myocardial oxidative stress and antioxidant capacity in the pathogenesis of myocardial injury in type 2 diabetes mellitus (T2DM) rats and provide a scientific basis for the treatment of T2DM. Methods Thirty-two SD rats were randomly divided into 4 groups, 8 weeks and 12 weeks in the control group, 8 weeks and 12 weeks in the diabetic group, with 8 rats in each group. Control group fed normal diet, streptozotocin (STZ) 50 mg / kg induced T2DM rat model. The content of nitric oxide (NO) in myocardium was measured by nitrate reductase method. The activity of nitric oxide synthase (NOS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by chemical colorimetry. Results The levels of NO, MDA and NOS in diabetic group increased at the 8th week and the 12th week, and the activity of SOD decreased. The difference was statistically significant (P <0.05, P <0.01). Conclusion With the prolongation of the course of T2DM rats, the myocardial antioxidant capacity gradually decreased, leading to oxidative stress injury in the myocardium.