黄芪多糖对力竭运动大鼠心肌细胞凋亡及BcL-2、Bax蛋白表达的影响  

Effects of acute exercise to exhaustion on BcL-2,Bax gene of rat, sheart after supplyment of astragalus polysaccharide

作　　者：马兰军[1] 田振军[2] 

机构地区：[1]西安建筑科技大学体育系,西安710055 [2]陕西师范大学体育学院,西安710062

出　　处：《华中师范大学学报（自然科学版）》2012年第2期214-217,共4页Journal of Central China Normal University：Natural Sciences

基　　金：基金项目：国家科技部主任基金项目（31040045）;国家自然科学基金项目（31040045）

摘　　要：为了探讨黄芪多糖（APS）对力竭运动大鼠机体的保护作用，通过建立大强度力竭运动大鼠模型，选取成年健康雄性SD大鼠24只，随机分为安静对照组，运动组和运动加药组，运动组和运动加药组按照训练模型进行为期6周的耐力训练，最后1次训练进行1次力竭运动，随后取心肌组织并进行样本处理．检测大鼠心肌MDA含量，用缺口末端标记法（TUNEL法）及免疫组织化学法检大鼠心肌细胞凋亡指数（AI）及BcL-2、Bax蛋白表达的变化．结果表明：运动组MDA含量、AI和BcL-2、Bax蛋白表达水平均明显高于安静对照组（P〈0．05）；与运动组比较，运动加药组MDA含量，AI与Bax蛋白表达水平均下降，而BcL-2蛋白表达水平显著增高（P〈O．05）．黄芪多糖可有效抑制力竭运动大鼠心肌细胞凋亡，此作用可能与其减轻氧化应激、上调BcL-2和下调Bax蛋白表达水平有关．To study the supplementary astragalus polysaccharide （APS） to exhaustion movement rats myocardial cell apoptosis, observe the influence of myocardial cell apoptosis BcL-2, the regulation of gene Bax changes, explore astragalus polysaccharide （APS） to exhaustion movement rats airframe of protection. By establishing high intensity exhaustion movement model of rats, the selection of adult health male SD rats 24 only randomly divided into quiet in the exercise group and control group, sports dosing group, the exercise group and exercise dosing groups according to training model sixweek endurance training, last training once exhaustion movement, exhaustion after motion myocardial organize and sample processing. Detection rats myocardial MDA content, using gap end labeling （TUNEL law） and the method of immunohis to chemistry methods were used by rats myocardial cell apoptosis I,ndex （AI） and BcL-2, Bax pro- tein expression changes. In the exercise group MDA content, AI and BcL-2, Bax protein expression levels were significantly higher in quiet in control group （P 〈 0.05）. Group compared with sports exercise dosing group MDA content, AI and Bax protein expression level decreased, and BcL-2 protein expression levels rose significantly （P〈 0.05）. Astragalus polysaccharide （APS） can restrain the movement exhaustion rats my- ocardial cell apoptosis, this function may reduce oxidatie stress, raised with BcL-2 and cut Bax protein expression level concerned.

关 键 词：黄芪多糖 力竭运动 心肌 细胞凋亡 BCL-2蛋白 BAX蛋白 

分 类 号：Q343.1[生物学—遗传学]