摘要
目的:探讨链脲佐菌素(STZ)诱导的不同周期糖尿病对心肌缺血/再灌注(I/R)损伤的影响及其与血浆一氧化氮(NO)变化的关系。方法:阻断和开放左冠状动脉前降支建立大鼠急性心肌I/R模型。分别用TTC染色测定大鼠心肌I/R后梗死面积;用硝酸还原酶法测定NO含量;用免疫印迹法定量分析代表细胞生存信号的磷酸化蛋白激酶B(P-Akt)的表达。结果:STZ处理后2周,糖尿病组(2WD+I/R)心肌梗死面积比相应周期对照组(2WC+I/R)明显缩小,STZ处理后16周(16WD+I/R),梗死面积比相应对照组(16WC+I/R)增加;血浆NO水平在2周糖尿病组中较对照组增高,但是在16周糖尿病组中较对照组显著减少;P-Akt在心肌的表达在2WD组比2WC组增加35%,在16WD组比16WC组明显减少。结论:STZ诱导的急、慢性期糖尿病对心肌I/R损伤呈现相反的作用。这可能是由于急、慢性期糖尿病相反的NO改变而引起的。
Objective To determine the effects of different-term STZ-induced diabetes on ischemia/reperfusion （I/R） injury of myocardium and if I/R injury is related to diabetes-induced alterations in NO levels. Methods A rat model of I/R injury was established by the occlusion and reperfusion of left descending coronary artery （LDCA）. Size of I/ R-induced infarct was determined using triphenyhetrazolium chloride （TTC） staining; NO production was quantified by nitrlte/nitrate colormetric method; Phosphorylation of protein kinase B （P-Akt） expression featuring cell survival signaling was quantified by Western blot analysis. Result Two weeks after STZ treatment, infarct size was decreased in the 2 weeks of diabetic hearts （2WD） as compared with time-matched control group （2WC）, whereas after 16 weeks of diabetes （16WD）, the infarct size was increased in the diabetic hearts as compared with the 16WC group. Plasma NO levels were increased in 2WD rats whereas NO levels were markedly decreased in 16WD group compared with time-matched controls. P-Akt expression was increased in 2WD group by 35% over 2WC values whereas there was a decrease in P-Akt expression in both 16WD and 16WC group. Conclusion Short- and long-term ST-Z-induced diabetes exert opposite effects on myocardial I/R injury, and these contradictory effects may depend on different alterations in NO levels.
出处
《实用医学杂志》
CAS
2006年第18期2092-2095,共4页
The Journal of Practical Medicine
关键词
糖尿病
心肌
再灌注损伤
一氧化氮
生存信号
Diabetes mellitus Myocardium Reperfusion injury Nitric oxide Survival signaling
