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类法尼醇X受体拮抗剂可减轻高脂载脂蛋白E基因敲除小鼠心肌缺血再灌注损伤
2013年
目的探讨类法尼醇x受体(FXR)拈抗剂对高脂载脂蛋白E(ApoE)基因敲除(ApoE_-/-)小鼠心肌缺血再灌注(I/R)损伤的影响及其机制。方法取雄性ApoE_-/-小鼠,分为3组:(1)标准ApoE_-/-组(n=18):予标准鼠料喂养12周后建立心肌I/R模型;(2)高脂ApoE_-/-组(n=22):予高脂鼠料(含1.25%胆固醇)喂养12周后建立心肌I/R模型;(3)高脂ApoE_-/-+FXR拮抗剂组(n=17):予高脂鼠料喂养12周后建立心肌I/R模型,心肌I/R前30min给予FXR拮抗剂Z—guggulsterone(100mg/kg)。荧光实时定量PCR(RT—qPCR)检测FXR基因变化,伊文斯兰及氯化三苯基四氮唑(TFC)双染色法检测心肌梗死面积,TUNEL法检测心肌细胞凋亡情况,酶联免疫吸附试验(ELISA)法测定心肌线粒体细胞色素C释放,荧光底物法检测caspase-9、12、8和3的活性,RT—qPCR检测BAX、BCL-2、CCAAT/增强子结合蛋白同源蛋白(CHOP)、自杀相关因子(Fas)和自杀相关因子配体(FasL)等基因的表达水平。结果高脂ApoE_-/-组小鼠心肌组织FXRmRNA表达水平显著高于标准ApoE_-/-组(P〈0.01)。高脂ApoE_-/-组小鼠心肌I/R诱导心肌梗死面积显著高于标准ApoE_-/-组[(62.1±7.0)%比(33.8±5.8)%,P〈0.01],心肌细胞凋亡指数亦显著高于标准ApoE_-/-组[(36.8±5.7)%比(17.2±3.8)%,P〈0.01]。高脂ApoE_-/-+FXR拮抗剂组小鼠心肌梗死面积则显著小于高脂ApoE_-/-组[(24.4±4.7)%比(62.1±7.0)%,P〈0.01],心肌细胞凋亡指数亦显著低于高脂ApoE_-/-组[(13.8±2.7)%比(36.8±5.7)%,P〈0.01],细胞凋亡的线粒体通路激活的标志物(线粒体细胞色素c释放、caspase-9以及BAX/BCL-2表达比例)和内质网应激通路的标志物(caspase-12活性以及CHOP表达)均较高脂ApoE_-/-组低(P均〈0.01),而膜受体死亡通路的标志物(
童欢单培仁赵怡超袁安彩何清幺天保应小盈卜军何奔
关键词:心肌再灌注损伤
Protective role of retinoid X receptor in H9c2 cardiomyocytes from hypoxia/reoxygenation injury in rats被引量:5
2014年
BACKGROUND: Retinoid X receptor(RXR) plays a central role in the regulation of intracellular receptor signaling pathways. The activation of RXR has protective effect on H2O2-induced apoptosis of H9c2 ventricular cells in rats. But the protective effect and mechanism of activating RXR in cardiomyocytes against hypoxia/reoxygenation(H/R)-induced oxidative iniury are still unclear.METHODS: The model of H/R injury was established through hypoxia for 2 hours and reoxygenation for 4 hours in H9c2 cardiomyocytes of rats. 9-cis-retinoic acid(9-cis RA) was obtained as an RXR agonist, and HX531 as an RXR antagonist. Cultured cardiomyocytes were randomly divided into four groups: sham group, H/R group, H/R+9-cis RA-pretreated group(100 nmol/L 9-cis RA), and H/R+9-cis RA+HX531-pretreated group(2.5 μmol/L HX531). The cell viability was measured by MTT, apoptosis rate of cardiomyocytes by flow cytometry analysis, and mitochondrial membrane potential(ΔΨm) by JC-1 fluorescent probe, and protein expressions of Bcl-2, Bax and cleaved caspase-9 with Western blotting. All measurement data were expressed as mean±standard deviation, and analyzed using one-way ANOVA and the Dunnett test. Differences were considered signif icant when P was <0.05.RESULTS: Pretreatment with RXR agonist enhanced cell viability, reduced apoptosis ratio, and stabled ΔΨm. Dot blotting experiments showed that under H/R stress conditions, Bcl-2 protein level decreased, while Bax and cleaved caspase-9 were increased. 9-cis RA administration before H/R stress prevented these effects, but the protective effects of activating RXR on cardiomyocytes against H/R induced oxidative injury were abolished when pretreated with RXR pan-antagonist HX531.CONCLUSION: The activation of RXR has protective effects against H/R injury in H9c2 cardiomyocytes of rats through attenuating signaling pathway of mitochondria apoptosis.
Pei-ren ShanWei-wei XuZhou-qing HuangJun PuWei-jian Huang
关键词:CARDIOMYOCYTESAPOPTOSISMITOCHONDRIA
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