摘要
目的:探讨阈下电刺激对大鼠缺血心肌细胞凋亡及bcl-2和bax表达的影响。方法:Wistar大鼠随机分为假手术组、急性心梗组、阈下电刺激组,假手术组手术不结扎,置入电极不给予电刺激;急性心梗组和阈下电刺激组采用左冠状动脉前降支结扎法建立大鼠急性心肌梗死模型,急性心梗组仅植入电极,不给予电刺激,阈下电刺激组在建立心肌梗死模型后,给予25 Hz、0.3 V阈下电刺激,TUNEL法检测3组大鼠心肌细胞凋亡,免疫组化和RT-PCR的方法检测心肌bcl-2及bax蛋白和mRNA的表达。结果:(1)与假手术组比较,急性心梗组、阈下电刺激组大鼠心肌细胞凋亡指数显著升高(P<0.05);与急性心梗组比较,阈下电刺激组大鼠心肌细胞凋亡指数降低(P<0.05)。(2)与假手术组比较,急性心梗组、阈下电刺激组大鼠心肌细胞bcl-2和bax蛋白和mRNA的表达显著升高(P<0.05);与急性心梗组比较,阈下电刺激组大鼠心肌细胞bcl-2蛋白和mRNA的表达显著升高,而bax基因表达显著降低(P<0.05)。结论:阈下电刺激能显著减少大鼠心肌梗死后缺血心肌细胞凋亡,其机制可能与上调bcl-2表达和下调bax表达有关。
Objective： To explore the effects of subthreshold electrical stimulation on cardiomyocytes apoptosis and gene expression of bcl-2 and bax in ischemic cardiomyocytes of rats. Methods： 18 rats were randomly divided into 3 groups：sham operation group （group S）, acute myocardial infarction （AMI） group （group A） and subthreshold electrical stimulation group （group E）. The left anterior descending coronary of rat hearts in group A and group E were ligated to establish AMI model. Elec- trodes were implanted into rats in the three group , but not giving electrical stimulation in group S and group A, and rats in group E were given subthreshold electrical stimulation of 25 Hz and 0.3 . Cardio- myocyte apoptosis was detected with TUNEL method, and the expressions of bcl-2 and bax were deter- mined by using immunohistochemistry and RT-PCR methods. Results： （1） Compared with group S, the apoptotic indexes of cardiomyocytes in group A and group E were increased significantly （P 〈 0. 05 ） ; Compared group A, the apoptotic indexes of cardiomyocytes in group E were decreased signifi-cantly （P 〈 0.05 ）. （2） Compared with group S, the expressions of bcl-2 and bax gene and protein in group A and group E were increased significantly （ P 〈 0.05 ） ; Compared with that of group A, the ex- pression of bcl-2 gene and protein in group E was increased significantly, while the expression of bax gene and protein was decreased significantly （ P 〈 0.05 ）. Conclusions： Subthreshold electrical stimu- lation can reduce the number of apoptotic cardiomyocytes in AMI rats, the mechanisms may be associ- ated with up-regulating the expression of bcl-2 and down-regulating the expression of bax.
出处
《贵阳医学院学报》
CAS
2014年第4期494-497,共4页
Journal of Guiyang Medical College
基金
贵州省科学技术基金项目黔科合丁字[2007]2089号
