rp105抑制tlr4信号通路对大鼠心肌缺血再灌注凋亡损伤的保护作用及其机制分析word论文.docxVIP

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rp105抑制tlr4信号通路对大鼠心肌缺血再灌注凋亡损伤的保护作用及其机制分析word论文.docx

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rp105抑制tlr4信号通路对大鼠心肌缺血再灌注凋亡损伤的保护作用及其机制分析word论文

缺血再灌注心肌细胞的凋亡损伤过程；(4) RP105 心肌过表达可抑制线粒体依赖性的凋亡级联反应，降低缺血再灌注诱导的心肌细胞凋亡；(5) RP105 可能通过抑制TLR4/P38MAPK/AP-1 信号通路活化，从而抑制大鼠心肌缺血再灌注损伤。关键词：RP105缺血再灌注损伤心肌细胞凋亡TLR4AbstractObjective The major aim of the present work was to provide molecular mechanistic by which RP105 protects cardiomyocytes from cell apoptosis during ischemic and ensuing reperfusion conditions via suppression TLR4-triggerred signaling pathways in rats.Methods 40 adult male Sprague-Dawley rats (SPF grade, weighting 220-250g) were randomly allocated into four equal groups(n=10):(1)normal non-ischemic group (Sham group); (2) myocardial I/R group( I/R group);(3) myocardial I/R with Ad-EGFP group(Ad-E group);(4) myocardial I/R with Ad-EGFP-RP105 group(Ad-E-R group). On the forth day after adenovirus or normal saline delivery, all of the rats underwent 30min of coronary occlusion followed by reperfusion for 4h with the exception of shamed group. Then, immunohistochemistry and fluorescence microscopy were approached for the expression of EGFP and RP105; Evans Blue/triphenyltetrazolium chloride (TTC) double-staining was performed to determinate the infarct area of myocardium; the in vivo terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) assay was used to detect the apoptotic cardiomyocytes; Real-time PCR was performed for the level of EGFP and RP105 mRNA. Moreover, we preferred to western blot analysis to assess the expression level of objective proteins in dissected myocardial tissue, such asBax、cytochrome c、Bcl-2、cleaved caspase-3、caspase-9、RP105、TLR4、P38MAPK、p-P38MAPK、c-Jun/AP-1 and p-c-Jun/AP-1.Results (1) Adenoviral transduction using both Ad-EGFP-RP105 and Ad-EGFP was sufficient to induce the expression of EGFP and RP105 in myocardium. (2) Relative tonon-ischemic sham control, myocardium from I/R、Ad-E and Ad-E-R groups showedenhanced levels of infracted area and apoptotic index. Furthermore, compared with sham group, increased levels of pro-apoptotic molecules, including Bax, cytochrome