带有caspase富集功能域的凋亡抑制因子对急性病毒性心肌炎小鼠心肌的保护作用

目的 研究急性病毒性心肌炎(AVMC)小鼠的带有caspase富集功能域的凋亡抑制因子(ARC)的表达及对心肌的保护.方法 将60只成功建立AVMC模型的小鼠随机分为ARC反义寡核苷酸组(A组)、ARC错义寡核苷酸组(B组)和生理盐水对照组(C组),每组20只.分期分别采集标本测定外周血心肌钙蛋白T(cTnT)、心肌钙蛋白I(cTnI)、肌酸激酶(CK)、肌酸激酶同功酶(CK-MB)水平和ARC、动力相关蛋白1(Drp1)表达等数据.结果 造模后第7、14、21天,3组外周血cTnT、cTnI、CK、CK-MB水平差异有统计学意义(P<0.05),C组与B组相近(P>0.05),但均低于A组(P<0.05).造模后第7天,3组ARC与Drp1蛋白表达水平差异有统计学意义(P<0.05),C组ARC表达与B组相近(P>0.05),但均高于A组(P<0.05),C组Drp1蛋白表达与B组相近(P>0.05),但均低于A组(P<0.05);造模后第14、21天3组ARC与Drp1蛋白表达水平差异无统计学意义(P>0.05).结论 小鼠发生AVMC后高表达的ARC可抑制心肌细胞凋亡,对心肌组织有保护作用.

Protective effect of ARC on myocardium in mice with acute viral myocarditis

Objective To investigate the expression of apoptosis inhibitory factor (ARC) and its protective effects on caspase in mice with acute viral myocarditis (AVMC).Methods Sixty AVMC mice were randomly divided into ARC antisense oligonucleotides (group A), ARC missense oligonucleotide group (groupB) and normal saline control group (groupC), with 20 mice in each group.Peripheral blood specimens in different stageswere collected for determination of cardiac troponin T (cTnT), cardiac troponin I (cTnI), creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and the level of ARC, dynamin related protein 1 (Drp1) expression data.Results On 7th, 14th, and 21stdays after modeling, the difference in cTnT, cTnI, CK and CK-MB levels in the peripheral blood of the three groups was statistically significant (P<0.05), and group C was similar to groupB (P>0.05), but lower than that of groupA.On 7th day after modeling, difference in ARC and Drp1 protein expression level in three groups was statistically significant (P<0.05), ARC in group Cwas similar to that in group B(P>0.05), but higher than that in group A (P<0.05);the expression of Drp1 protein in groupC was similar to that in group B(P>0.05), but lower than that in group A(P<0.05).ARC and Drp1 protein expression level on 14th and 21stdays after the modeling in three groups showed no significant difference (P>0.05).Conclusion The high expression of AVMC can inhibit the apoptosis of myocardial cells and protect the myocardium after ARC.