PI3K-Akt、mito-KATP通道及mPTP在阿托伐他汀后处理减轻大鼠心肌缺血再灌注损伤中的作用

被引：17

作者：

刘春伟 ^{[1
]}

丛洪良 ^{[1
]}

于雪芳 ^{[2
]}

韩薇 ^{[3
]}

机构：

[1] 天津市胸科医院心内科

[2] 天津医科大学总医院心内科

[3] 首都医科大学附属北京安贞医院心外科

来源：

天津医药 | 2015年 / 43卷 / 01期

关键词：

心肌再灌注损伤; 1-磷脂酰肌醇3-激酶; KATP通道; 腺苷三磷酸; 线粒体; 细胞膜通透性; 阿托伐他汀后处理;

D O I：

暂无

中图分类号：

R96 [药理学];

学科分类号：

100602 ; 100706 ;

摘要：

目的观察阿托伐他汀(ATV)后处理对离体大鼠心肌缺血再灌注损伤的保护作用,探讨磷脂酰肌醇-3-激酶-蛋白激酶B(PI3K-Akt)、线粒体ATP敏感性钾通道(mito-KATP通道)及线粒体膜通透性转换孔(m PTP)在其中的作用。方法将雄性Wistar大鼠随机分为对照组(I/R组)、阿托伐他汀后处理组(ATV组)、ATV复合PI3K抑制剂LY294002组(ATV+LY294002组)、LY294002组、ATV复合mito-KATP通道抑制剂5-羟葵酸(5-HD)组(ATV+5-HD组)、5-HD组、ATV复合m PTP开放剂苍术甙(ATR)组(ATV+ATR组)、ATR组,乙醇对照组。进行30 min缺血,120min再灌注。观察各组心肌梗死范围,血流动力学指标,肌酸磷酸激酶同工酶(CK-MB)和乳酸脱氢酶(LDH)含量,烟酰胺腺嘌呤二核苷酸(NAD+)含量,心肌Akt和磷酸化Akt表达水平。结果 ATV组心肌梗死范围、LDH、CK-MB较I/R组下降(P<0.05),心肌NAD+含量较I/R组增加(P<0.05);ATV+LY294002组、ATV+5-HD组,ATV+ATR组心肌梗死范围、CK-MB、LDH,NAD+较I/R组差异无统计学意义。ATV组较I/R组血流动力学指标改善。Western blot显示ATV组、ATV+5-HD组和ATV+ATR组磷酸化Akt表达较I/R组增加,ATV+LY-294002组、LY-294002组、ATR组、5-HD组磷酸化Akt表达与I/R组相比无增加。结论阿托伐他汀后处理通过激活PI3K-Akt、促进mito-KATP通道开放,抑制m PTP开放,产生心肌保护作用。

引用

页码：46 / 50

页数：5

共 11 条

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