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蜂胶黄酮对小鼠缺血再灌注后心肌线粒体损伤的保护作用 被引量:5

Protective effect of propolis flavonoids on myocardium mitochondrial injury induced by ischemia/reperfusion in rats
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摘要 目的:探讨蜂胶黄酮对小鼠力竭游泳后心肌线粒体缺血再灌注损伤的保护作用。方法:将70只小鼠随机分为安静组(A组)、力竭对照组(B组)和力竭给药组(C组)。A、B组常规喂养,C组灌喂蜂胶黄酮液。B、C组进行4周递增负荷游泳训练,并于最后一次训练至力竭,测定其安静时、力竭后即刻、6小时和24小时心肌线粒体超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、总-抗氧化能力(T-AOC)、丙二醛(MDA)、Ca2+、磷脂酶A2(PLA2)等指标。结果:缺血再灌注后B组小鼠心肌线粒体中抗氧化物质(SOD、GSH-Px、T-AOC)活性显著下降,MDA含量、PLA2活性显著升高,心肌钙离子明显超载,尤以力竭运动后6h最为显著;而补充蜂胶黄酮的C组与B组相比,抗氧化物质活性显著提高,自由基MDA含量、PLA2活性显著下降,钙离子明显减少。结论:蜂胶黄酮对缺血再灌注损伤的心肌线粒体有积极的保护作用。 The thesis aimed at studying the protective effect of propolis flavonoids on the myocardium mitochondrial injury induced by ischemic/reperfusion in rats after exhausted exercise.Methods of the thesis were that 70 rats were divided into three groups randomly,Group A: sedentary group;Group B: exhausted exercise group;Group C: exhausted exercise and drug group.Group A,B were fed with normal diet,Group C was treated with propolis flavonoids.Group B,C were swimming by increasing exercises loads gradually for four weeks,and performing an exhaustive swimming exercise at last.Then the SOD,GSH-Px,T-AOC,MDA,PLA2,Ca2+ level of myocardium mitochondrial were measured at quiet,right after exhaustive exercise,6h and 24h after exhaustive exercise.It was shown that content of Myocardium mitochondrial MDA,PLA2,Ca2+ level were remarkably increased in Group B,while the activities of anti-oxide(SOD,GSH-Px and T-AOC) were decreased in the same time,and these changes reach the maximum at 6h after exhaustive exercise.Compared with Group B,the activities of anti-oxide of Group C has obviously been improved,content of MDA,PLA2,Ca2+ level ware remarkably declined.It is concluded that propolis flavonoids has a protective function on the injury of myocardium mitochondria induced by ischemic/reperfusion in rats.
作者 潘燕 彭彦铭
出处 《武汉体育学院学报》 CSSCI 北大核心 2011年第8期36-38,43,共4页 Journal of Wuhan Sports University
基金 湖北省教育厅科技处重点项目(D20092201)
关键词 蜂胶黄酮 缺血再灌注 心肌线粒体 损伤 propolis flavonoids schemia/reperfusion myocardium mitochondrial injury
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