地塞米松对大鼠缺血再灌注心肌细胞凋亡及HSP72、NF-κB表达的影响  

Effects of dexamethasone on myocardial apoptosis and expressions of HSP72,NF-κB in rat hearts during ischemia/reperfusion

作　　者：庄梅[1] 方颖[1] 吴立荣[1] 雷大卫[1] 

机构地区：[1]贵阳医学院附属医院心脏内科,贵州贵阳550004

出　　处：《中国老年学杂志》2008年第15期1467-1469,共3页Chinese Journal of Gerontology

基　　金：贵州省科学技术基金〔黔科合J字(2007)2099〕

摘　　要：目的探讨地塞米松预处理对大鼠缺血再灌注(I/R)心肌细胞凋亡及热休克蛋白72(HSP72)、核因子κB(NF-κB)表达水平的影响。方法SD大鼠随机分成地塞米松组和对照组,分别予地塞米松和生理盐水预处理。预处理后构建Langendorff离体心脏I/R动物模型,测定冠状动脉流出液肌酸激酶MB同工酶(CK-MB)的漏出率及观察心肌超微结构的变化;原位末端标记(TUNEL)法检测心肌细胞凋亡;Western印迹法检测HSP72表达;免疫组化法检测NF-κB的活化水平。结果与对照组相比,地塞米松组冠状动脉流出液CK-MB的漏出率降低(P<0.05);超微结构的损伤减轻;细胞凋亡指数及NF-κB表达减少(P<0.01),HSP72表达增加(P<0.05)。结论地塞米松上调心肌HSP72及下调NF-κB表达可能与其抑制I/R心肌细胞凋亡有关。Objective To explore the effects of dexamethasone（DEX） proconditioning on myocardial apoptotic and heat-shock proteins（ HSP72）, nuclear factor-kappa B （NF-κB） expression in rat hearts during ischemia/reperfusion （I/R）. Methods Spragne-Dawley rats were divided randomly into DEX and control group, the rats had been pretreated with DEX or sodium chloride before their hearts were separated for Langendorff perfusion and for I/R. The levels of CK-MB in the coronary artery flow were measured and the myocardial ultra- structures were also examined. Apoptosis was measured by TUNEL staining method. HSP72 was assessed by Western blot. NF-KB activation was examined by immunohistochemistry. Results Compared with control group, I/R injury of myocardial uhrastructure was decreased. The apoptotic index, the level of CK-MB and the activation of NF-KB were significantly decreased （ P 〈 0. 01, P 〈 0. 05 ）. The expression of HSP72 was significantly increased（P 〈 0. 05 ）. Conclusions DEX induces up-regulation of HSP72 and down-regulation of NF-κB, which may inhibit myocardial apoptosis after I/R in rat.

关 键 词：地塞米松 缺血再灌注 凋亡 热休克蛋白70 核因子ΚB 

分 类 号：R363[医药卫生—病理学]