本文選題：病毒性心肌炎 + 硒　； 參考：《吉林大學(xué)學(xué)報(bào)(醫(yī)學(xué)版)》2016年01期

【摘要】：目的:探討硒對(duì)病毒性心肌炎(VMC)小鼠心肌細(xì)胞凋亡的抑制作用,闡明其對(duì)PI3K-Akt信號(hào)傳導(dǎo)通路中Akt、磷酸化Akt(p-Akt)及其下游靶基因編碼的Bax和Bcl-2蛋白的作用機(jī)制。方法:60只BALB/c小鼠隨機(jī)分為正常對(duì)照組、病毒對(duì)照組和硒干預(yù)組(n=20)。正常對(duì)照組小鼠連續(xù)3d腹腔注射不含病毒的培養(yǎng)液200μL;病毒對(duì)照組小鼠腹腔注射100半數(shù)組織培養(yǎng)感染劑量(TCID50)柯薩奇病毒B組病毒(CVB3)液200μL,連續(xù)3d;硒干預(yù)組小鼠在病毒對(duì)照組同樣的處理后灌胃給予100μg·kg-1亞硒酸鈉,每日1次,連續(xù)處理14d。接種CVB3的第15天處死小鼠,TUNEL法檢測(cè)心肌細(xì)胞的凋亡情況,光鏡下觀察心肌病理變化,Western blotting法檢測(cè)心肌細(xì)胞中Akt、p-Akt、Bcl-2、Bax和Cleaved caspase-3蛋白表達(dá)水平。結(jié)果:與病毒對(duì)照組比較,硒干預(yù)組小鼠生存率明顯升高(P0.01)。硒干預(yù)組小鼠的心肌病理改變較病毒對(duì)照組減輕。硒干預(yù)組小鼠心肌細(xì)胞凋亡率低于病毒對(duì)照組(P0.01)。與病毒對(duì)照組比較,硒干預(yù)組小鼠心肌細(xì)胞中p-Akt、Bcl-2蛋白表達(dá)水平增加,Bax、Cleaved caspase-3蛋白表達(dá)水平明顯降低,Bax/Bcl-2蛋白比值下降(均P0.01)。結(jié)論:硒對(duì)CVB3感染導(dǎo)致的VMC小鼠心肌細(xì)胞有保護(hù)作用,其作用機(jī)制與硒通過(guò)活化心肌細(xì)胞的PI3K-Akt信號(hào)通路、調(diào)控其下游Bcl-2和Bax蛋白表達(dá)和抑制心肌細(xì)胞凋亡有關(guān)。
[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.
【作者單位】： 吉林大學(xué)第二醫(yī)院兒科;
【基金】：吉林省科技廳青年基金資助課題(20140520022JH) 吉林省長(zhǎng)春市科技局科研基金資助課題(2012150-12SF78)
【分類號(hào)】：R965

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本文編號(hào)：1952691