锰对糖尿病大鼠心肌SOD活性与MDA含量的影响  

Effect of Manganese on SOD Activity and MDA Level of Diabetic Rat

作　　者：康艳萍[1] 王国秋[1] 齐志敏[1] 李淑云[1] 马克玲[1] 白秀珍[1] 

机构地区：[1]锦州医学院,锦州121000

出　　处：《数理医药学杂志》2006年第6期589-591,共3页Journal of Mathematical Medicine

摘　　要：目的:观察锰剂对Ⅱ型糖尿病大鼠心肌的保护作用并探讨其机制。方法:以高糖高脂饲料饲喂后的雄性SD大鼠小剂量尾静脉注射STZ诱导Ⅱ型糖尿病模型,将实验动物分为正常组、糖尿病组、补锰组,检测各组喂养6周、10周、14周的血糖水平,检测第14周后心肌组织中丙二醛(M DA)含量及锰-超氧化物歧化酶(M n-SOD)活性。结果:与糖尿病组相比,补锰各组心肌组织M DA含量明显下降(P<0.01),而M n-SOD活性明显上升(P<0.01、P<0.005和P<0.05)。结论:补锰可以改善Ⅱ型糖尿病大鼠的心肌抗氧化能力。Objective： Protection roles of Manganese on myocardium of Ⅱ diabetic rat were observed and their mechanisms were explored. Method： Experimental animals Were divided in three groups： the control groups, the diabetic groups and supplying Manganese groups. When the rats were fed in 6 weeks, 10 weeks and 14 weeks, we detected blood sugar level of every groups. In 14 weeks, MDA content of myocardium tissue and Mn-SOD activities were examined. Result： Compare to the diabetic groups, supplying Manganese groups can decrease significantly MDA（P〈0. 01） content of myocardium tissue, but increase significantly Mn-SOD （P 〈 0. 01, P 〈 0. 005 和 P 〈 0. 05） activities. Conclusion： supplying Manganese can improve myocardial injury of Ⅱ diabetes. Roles of supplying Manganese were related to accelerate anti-oxidation action.

关 键 词：锰 糖尿病 心肌 超氧化物岐化酶 丙二醛 

分 类 号：R962[医药卫生—药理学]