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首页> 外文期刊>Journal of research in medical sciences : >ATORVASTATIN INHIBITS FAS EXPRESSION IN ISCHEMIA-REPERFUSION INDUCED MYOCARDIAL CELL INJURY
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ATORVASTATIN INHIBITS FAS EXPRESSION IN ISCHEMIA-REPERFUSION INDUCED MYOCARDIAL CELL INJURY

机译:阿托伐他汀抑制缺血再灌注诱导的心肌细胞损伤中FAS表达。

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BACKGROUND: Atorvastatin has been shown to be cardio protective in ischemia-reperfusion (I/R) injury. Inhibition of Fas expression prevents I/R induced apoptosis. However, the influence of atorvastatin on Fas expression in I/R injury was not studied. Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. METHODS: Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. Apoptosis of the cardiomyocytes was observed under electron microscopy and determined by optic microscopy with TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining. To detect the expression of Fas in the cardiomyocytes, immunohistochemistry method was used. Image analysis system was used to quantitatively estimate the positive metric substances of immunohistochemistry through the mean optic density. RESULTS: Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and weren’t observed in the sham-operated group. Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. CONCLUSION: Up regulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression.
机译:背景:阿托伐他汀在缺血再灌注(I / R)损伤中具有心脏保护作用。 Fas表达的抑制可防止I / R诱导的细胞凋亡。但是,尚未研究阿托伐他汀对I / R损伤中Fas表达的影响。因此,我们设计本研究以观察阿托伐他汀对急性I / R体内心肌细胞凋亡和Fas表达的影响。方法:选择Wistar大鼠30只,分为急性缺血再灌注(I / R)组,急性缺血再灌注3组,每组10只,分别用阿托伐他汀组和假手术组治疗。在电子显微镜下观察心肌细胞的凋亡,并通过光学显微镜用TUNEL(末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记)染色来确定。为了检测Fas在心肌细胞中的表达,使用了免疫组织化学方法。使用图像分析系统通过平均光密度定量估计免疫组化的阳性指标物质。结果:缺血再灌注组缺血区域发现大量凋亡心肌细胞,而假手术组未观察到。与假手术组相比,缺血再灌注组中的Fas表达显着较高,但与I / R组相比,在阿托伐他汀治疗组中Fas表达显着降低。结论:上调心肌缺血再灌注过程中Fas表达可诱导心肌细胞凋亡,阿托伐他汀可通过抑制Fas表达显着抑制心肌细胞凋亡。

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