运动干预糖尿病心肌病的分子机制研究

目的:观察链脲佐菌素诱导的糖尿病大鼠心肌组织中NADPH氧化酶表达的变化,探讨运动对NADPH氧化酶的影响。方法:大鼠糖尿病模型建立成功1周后,测定糖尿病对心肌组织中NADPH氧化酶亚基表达的影响,测定8周的运动能否有效影响NADPH氧化酶亚基的表达;观测糖尿病对心肌胶原蛋白表达的影响,8周运动是否能够影响胶原蛋白的表达。结果:糖尿病导致心室NADPH氧化酶亚基p47~(phox)和gp91~(phox)表达增加,而8周运动能够抑制这2种亚基表达的增加;糖尿病引起心房肌p47~(phox)表达显著增加,运动抑制其增加;糖尿病大鼠心肌胶原蛋白Ⅲ水平显著增加,运动降低胶原蛋白的增加。结论:运动减低糖尿病大鼠心脏p47~(phox)和gp91~(phox)的表达。这可能是改善心内基质的重要机制,因此运动干预糖尿病心肌病的一个有效机制可能是通过抑制心肌氧化应激和降低胶原蛋白的表达。

Molecular mechanism of exercise intervention in diabetic cardiomyopathy in rats

AIM:To investigate the effect of streptozotocin-induced diabetes on the expression of NADPH oxidase,and to determine the effect of exercise on the expression of NADPH oxidase.METHODS:One weeks after successful modeling,the effect of diabetes mellitus on the expression of NADPH oxidase subunits in the cardiac tissue was determined.The effect of exercise for 8 weeks on the protein expression of NADPH oxidase subunits and the effect of diabetes on the protein expression of collagen in the heart were observed,and whether 8 weeks of exercise affected the expression of collagen were also measured.RESULTS:Diabetes mellitus resulted in the increased expression of NADPH oxidase subunits p47^phox and gp91^phox in the cardiac ventricle,and exercise for 8 weeks inhibited the increase in the expression of NADPH oxidase subunits p47^phox and gp91^phox.Diabetes mellitus significantly increased the expression of p47^phox in the atrial muscle,while exercise inhibited this increase.Diabetes mellitus significantly increased the levels of cardiac collagen Ⅲ,while exercise reduced the increase in collagen protein.CONCLUSION:Reduction of diabetic rat heart p47^phox and gp91^phox expression by effective exercise therapy may be an important mechanism of improving the cardiac matrix by inhibiting myocardial oxidative stress and decreasing collagen expression,thus preventing diabetic cardiomyopathy.