硒对病毒性心肌炎小鼠心肌细胞凋亡的抑制作用及其作用机制

发布时间：2018-05-29 22:25

本文选题：病毒性心肌炎 + 硒　；参考：《吉林大学学报(医学版)》2016年01期

【摘要】：目的:探讨硒对病毒性心肌炎(VMC)小鼠心肌细胞凋亡的抑制作用,阐明其对PI3K-Akt信号传导通路中Akt、磷酸化Akt(p-Akt)及其下游靶基因编码的Bax和Bcl-2蛋白的作用机制。方法:60只BALB/c小鼠随机分为正常对照组、病毒对照组和硒干预组(n=20)。正常对照组小鼠连续3d腹腔注射不含病毒的培养液200μL;病毒对照组小鼠腹腔注射100半数组织培养感染剂量(TCID50)柯萨奇病毒B组病毒(CVB3)液200μL,连续3d;硒干预组小鼠在病毒对照组同样的处理后灌胃给予100μg·kg-1亚硒酸钠,每日1次,连续处理14d。接种CVB3的第15天处死小鼠,TUNEL法检测心肌细胞的凋亡情况,光镜下观察心肌病理变化,Western blotting法检测心肌细胞中Akt、p-Akt、Bcl-2、Bax和Cleaved caspase-3蛋白表达水平。结果:与病毒对照组比较,硒干预组小鼠生存率明显升高(P0.01)。硒干预组小鼠的心肌病理改变较病毒对照组减轻。硒干预组小鼠心肌细胞凋亡率低于病毒对照组(P0.01)。与病毒对照组比较,硒干预组小鼠心肌细胞中p-Akt、Bcl-2蛋白表达水平增加,Bax、Cleaved caspase-3蛋白表达水平明显降低,Bax/Bcl-2蛋白比值下降(均P0.01)。结论:硒对CVB3感染导致的VMC小鼠心肌细胞有保护作用,其作用机制与硒通过活化心肌细胞的PI3K-Akt信号通路、调控其下游Bcl-2和Bax蛋白表达和抑制心肌细胞凋亡有关。
[Abstract]:Aim: to investigate the inhibitory effect of selenium on apoptosis of cardiomyocytes in mice with viral myocarditis and to elucidate the mechanism of its effect on Bax and Bcl-2 proteins encoded by Bax and Bcl-2 in PI3K-Akt signal transduction pathway. Methods 60 BALB/c mice were randomly divided into normal control group, virus control group and selenium intervention group. Mice in the control group were intraperitoneally injected with 200 渭 L of virus-free culture medium for 3 days, while mice in the virus control group were given 100% intraperitoneal injection of TCID50) 200 渭 L of CVB3) solution of Coxsackie virus B group for 3 days; mice in the selenium intervention group were treated with the virus for 3 days. In the control group, 100 渭 g kg-1 sodium selenite was given intragastrically after the same treatment. Once a day, continuous treatment for 14 days. On the 15th day after inoculation of CVB3, the apoptosis of cardiomyocytes was detected by Tunel method. The pathological changes of myocardium were observed under light microscope. The expression of Akttip-Aktna-Bcl-2mBax and Cleaved caspase-3 protein in cardiomyocytes were detected by Western blotting method. Results: compared with the virus control group, the survival rate of mice in the selenium intervention group was significantly higher than that in the virus control group. The pathological changes of myocardium in selenium intervention group were less than those in virus control group. The apoptosis rate of myocardial cells in selenium intervention group was lower than that in virus control group (P 0.01). Compared with the control group, the expression of p-Aktbutathione Bcl-2 protein in the myocardial cells of mice treated with selenium increased the expression level of Bax-Cleaved caspase-3 protein decreased significantly (P 0.01). Conclusion: selenium has protective effect on cardiomyocytes induced by CVB3 infection in VMC mice. The mechanism is related to the regulation of Bcl-2 and Bax protein expression and the inhibition of cardiomyocyte apoptosis by selenium through activating the PI3K-Akt signaling pathway of cardiomyocytes.
【作者单位】：吉林大学第二医院儿科;
【基金】：吉林省科技厅青年基金资助课题(20140520022JH) 吉林省长春市科技局科研基金资助课题(2012150-12SF78)
【分类号】：R965

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