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作 者:任小宇[1] REN Xiao-yu(School of Medicine,Eastern Liaoning University,Dandong 118001,China)
机构地区:[1]辽东学院医学院
出 处:《辽东学院学报(自然科学版)》2019年第4期251-256,共6页Journal of Eastern Liaoning University:Natural Science Edition
摘 要:为了研究三七茎叶皂苷(PnGL)对大鼠离体心脏缺血/再灌注损伤模型心肌细胞凋亡的保护作用机制,采用TUNEL和免疫印迹(Western blot)蛋白方法检测细胞凋亡及凋亡基因蛋白Bcl-2、Bax、ERK1/2等相关凋亡通路,观察PnGL对心脏缺血/再灌注损伤后心肌细胞凋亡的保护作用机制。TUNEL结果显示,正常细胞核形态大小较为一致、荧光较弱,而凋亡细胞核呈高亮;空白对照组可见少量TUNEL阳性细胞;模型组阳性细胞显著增加;给予PnGL后凋亡细胞所占比例随着药物浓度的增加而明显下降。Western blot实验结果显示,与空白对照组比较,缺血/再灌注组中心肌细胞Bcl-2表达明显降低,Bax表达明显增加,ERK1/2和p-ERK1/2表达明显降低;给予PnGL后,Bcl-2表达明显升高,Bax表达明显降低,ERK1/2和p-ERK1/2表达明显升高。因此,PnGL对缺血再灌注诱导的心肌细胞凋亡具有保护作用,其保护作用可能与激活ERK1/2细胞凋亡保护通路、从而调节Bcl-2和Bax的表达有关。To investigate protective effects and the underlying mechanisms of Panax notoginsegnoside of leaves(PnGL)on ischemia/reperfusion and against ischemia/reperfusion-induced apoptosis injury in isolated rat heart,terminal deoxynucleotidy1 transferase-mediated dUTP nick end labeling(TUNEL)and western blot were designed in experiment to detect cardiomyocyte apoptosis and the pathway of apoptosis and the related proteins including Bcl-2,Bax,ERK1/2 and so on.Heart globe ischemia/reperfusion treatment caused severe injury to the myocardial tissue,which was accompanied by apoptosis,as revealed by analysis of TUNEL detection and Bcl-2,Bax protein expression by western blot detection.Model group showed the apparently increased apoptosis rate,western bolt assay showed increased protein expression of Bcl-2,Bax,ERK1/2 and p-ERK1/2.However,PnGL significant decreased cardiomyocyte apoptosis rate and protein expression of Bcl-2,Bax,ERK1/2 and p-ERK1/2.Therefore,PnGL prevents I/R-induced apoptosis in cardiomyocyte by reducing cardiomyocyte apoptosis rate and modulating the ERK1/2 pathways.
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