摘要
目的:通过建立Wistar大鼠2型糖尿病(T2DM)动物模型,观察T2DM大鼠心肌细胞凋亡及游泳训练对该凋亡事件的保护作用,并探讨其内在影响机制.方法:实验材料Wistar大鼠60只,造模完成后随机分成3组,1)正常对照组(CON);2)Diabetes模型组(DI);3)游泳运动组(DI+SEX),每组15只.游泳训练共计8周.结果:T2DM造成心肌组织Bcl-2水平降低,Bax水平升高;线粒体内及胞浆蛋白中Bax/Bcl-2比值升高,促凋亡物质细胞色素c(Cyt c)向胞浆释放增多(P<0.01);糖原合成激酶3β(GSK-3β)磷酸化水平升高(P<0.05).另外,T2DM引起胰岛素受体亚型1(IR1)水平降低(P<0.05),失活PI3K-Akt信号级联.相对地,游泳训练可明显抑制Bax/Bcl-2水平升高及GSK-3β磷酸化水平(P<0.05),显著性提高PI3K,Akt蛋白磷酸化及胰岛素受体IR1水平(P<0.05).虽对IR2水平有所提高,但无统计学意义.结论:游泳训练能有效抑制T2DM引起的Wistar大鼠心肌细胞凋亡.其抗凋亡作用可能是通过,至少部分通过上调IR1受体水平,激活PI3K-Akt生存通路,下调其下游关键蛋白GSK-3β磷酸化水平而实现.这表明游泳训练可以有效对抗T2DM引起的细胞凋亡事件的发生.
Purpose：Through establishing diabetes animal model（T2DM）,it was observed that T2DM caused myocardial apoptosis and the preservation induced by swimming training,and further the involved anti-apoptosis mechanism is explored.Method：After the model was established,Wistar rats total of 60 were randomly divided into three groups,1）normal control group（CON）;2）Diabetes model group（DI）;3）Swimming exercise group（DI＋SEX）,n=15 in each group.Swimming training duration lasted for 8 weeks.Results：T2DM could reduce the contents of Bcl-2,increase Bax levels both in cytoplasm and mitochondria.Rupture of mitochondrial membrane initiated Cytochrome c（Cyt c）and the release into cytoplasm;glycogen synthase kinase 3β（GSK-3β）phosphorylation levels was noteworthy higher than that of other two groups（P〈0.05）.Meanwhile,the results also showed that insulin receptor subtype 1（IR1）expression was down-regulated（P〈0.05）and PI3K-Akt signal cascades were inactivated.Correspondingly,swimming exercise could decline the ratio of Bax/Bcl-2,considerably improve the survival pathway and further activate GSK-3β protein phosphorylation（P〈0.05）.In addition,swimming exercise also could augment insulin receptor IR1（P〈0.05）contents.Although the level of IR2 was enhanced,there is no divergence for statistics.Conclusion：Swim training can effectively inhibit type 2 diabetes-induced myocardial apoptosis in Wistar rats.This anti-apoptotic effect may be through,at least in part,increasing the contents of IR1 receptor,and thereby activate PI3K-Akt signal cascade and further decline the phosphorylation expression of its key downstream of protein-GSK-3β,suggesting that swimming training may be an appropriate modality for combating with myocardial cell damage caused by T2DM.
出处
《晓庄学院自然科学学报》
CAS
北大核心
2012年第3期71-77,共7页
Journal of Natural Science of Hunan Normal University
基金
河南省科技攻关资助项目(112102310694)
关键词
2型糖尿病
游泳训练
心肌细胞凋亡
生存通路
糖原合成激酶3β
胰岛素受体
type 2 diabetes； swimming training； myocardial apoptosis； survival pathway； glycogen synthase kinase 3β； insulin receptor
