【摘 要】
：
目的：观察Salubrinal(Sal)对缺血诱发心力衰竭大鼠心功能的作用及心肌细胞凋亡和内质网应激的影响,探讨内质网应激诱发的心肌细胞凋亡在Sal改善心力衰竭大鼠心功能中的作
【机 构】
：
河北中医学院基础医学院生物化学教研室石家庄050200;050200石家庄,河北中医学院河北中医学院基础医学院生物化学教研室石家庄050200;210029南京市,江苏省临床医学研究院河北中医学院基础
【出 处】
：
2015全国中医药生物化学与分子生物学年会
论文部分内容阅读
目的：观察Salubrinal(Sal)对缺血诱发心力衰竭大鼠心功能的作用及心肌细胞凋亡和内质网应激的影响,探讨内质网应激诱发的心肌细胞凋亡在Sal改善心力衰竭大鼠心功能中的作用.方法：将8周龄雄性SD大鼠经冠状动脉结扎制做心肌梗塞心力衰竭模型,随机分为4组：假手术组,心力衰竭未治疗组,Sal治疗组和二甲基亚砜(Dimethyl sulfoxide,DMSO)治疗组.应用超声心动图于术后30min和8周分别检测心功能指标,8周末处死各组大鼠进行心指数的测定,并检测心肌细胞凋亡,内质网应激标志蛋白和凋亡信号通路蛋白的表达.结果：与假手术组相比,心力衰竭未治疗组大鼠心功能显著下降,心肌细胞凋亡数目增加,B型脑利钠肽(brain natriuretic peptide,BNP)表达升高,内质网应激标志蛋白钙网蛋白(calreticulin,CRT)和磷酸化型真核细胞翻译起始因子2α(phospho-eukaryotic translation initiation factor 2 subunit α,p-eIF2α)表达上调,内质网应激介导的凋亡信号通路caspase-12的表达上调(均为P<0.05).与心力衰竭未治疗组相比,Sal治疗可显著改善心力衰竭大鼠的心功能,明显抑制心肌细胞的凋亡,BNP表达下降,显著下调CRT和p-eIF2α的表达,下调内质网应激介导的凋亡信号通路caspase-12的表达(均为P<0.05).结论：心力衰竭时内质网应激反应被激活,心肌细胞凋亡增加,进而使心功能显著下降.Sal可通过抑制内质网应激反应介导的凋亡信号通路caspase-12的表达减轻心肌细胞凋亡,从而改善心功能.
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