Research Article

富氢水对心肌缺血再灌注损伤大鼠PI3K / AKT信号通路的影响

卷 20, 期 5, 2020

页: [396 - 406] 页: 11

弟呕挨: 10.2174/1566524019666191105150709

open access plus

摘要

背景:在遭受心肌缺血再灌注损伤(MIRI)的大鼠中研究了富氢水对PI3K / AKT介导的细胞凋亡的影响。 方法:将60只大鼠随机分为富氢水组和对照组。将心脏取出并固定在Langendorff装置中。对照组的心脏灌注K-R溶液,而富氢水组的心脏灌注K-R溶液+富含氢的水。然后将两个治疗组随机分为缺血前期,缺血期和再灌注期组(每组10只),分别进行反向灌注10分钟,正常治疗20分钟和再灌注20分钟。 。采用RT-qPCR,免疫组化(IHC)和Western blotting检测各组PI3K,AKT,p-AKT,FoxO1,Bim和Caspase-3的mRNA和蛋白表达水平。通过分光光度法检测Caspase-3活性。 结果:与缺血前和缺血后亚组相比,在富氢水组中,PI3K / AKT信号通路被显着激活,并且FoxO1,Bim和Caspase-3 mRNA和蛋白质水平显着降低。与相应对照组相比,缺血再灌注富氢水组中PI3K,AKT和p-AKT mRNA和蛋白表达水平升高,而FoxO1,Bim和Caspase-3表达水平显着降低(P < 0.05)。 结论:富氢水可以激活PI3K / AKT信号通路,减轻离体大鼠心脏的缺血再灌注损伤,并抑制心肌细胞凋亡。

关键词: 富氢水,心肌缺血-再灌注损伤,PI3K / AKT信号通路,FoxO1,Bim,Caspase-3,心肌细胞凋亡。

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