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作 者:刘书宇[1] 汤沂[1] 李贺娟 刘晶[1] 宫剑滨[1] LIU Shu-yu;TANG Yi;LI He-juan;LIU Jing;GONG Jian-bin(Department of Cardiology,General Hospital of Eastern Theater Command,PLA,Nanjing 210002,Jiangsu,China;Jiangsu Key Laboratory of Drug Screening,China Pharmaceutical University,Nanjing 210009,Jiangsu,China)
机构地区:[1]东部战区总医院(原南京军区南京总医院)心血管内科,南京210002 [2]中国药科大学药物科学研究院,南京210009
出 处:《医学研究生学报》2022年第12期1237-1243,共7页Journal of Medical Postgraduates
基 金:国家自然科学基金(81773963,81900409)。
摘 要:目的 线粒体自噬在心肌缺血再灌注损伤中起着重要作用,文章探讨了比索洛尔是否通过Drp1/Pink1/Parkin通路保护心肌细胞缺血/再灌注(I/R)损伤。方法 建立缺氧/复氧细胞模型,H9c2细胞缺氧6 h,复氧12 h。实验分为4组:对照组、缺氧/复氧组、缺氧/复氧+比索洛尔组、比索洛尔组。建立Drp1低表达的慢病毒载体(Drp1-siRNA),分别检测细胞活力、凋亡、线粒体分裂和自噬蛋白表达变化。结果 心肌细胞建立缺氧/复氧细胞模型后,经比索洛尔处理后,细胞存活率上升至83.25%±2.3%(P<0.05);细胞凋亡率减少30%(P<0.05);比索洛尔还可以降低Drp1的表达(P<0.05),增加LC3、Beclin1、Pink1和Parkin的表达(P<0.05)。Drp1-siRNA实验结果表明,与scramble处理相比,Drp1-siRNA处理减少了缺氧/复氧诱导的H9c2细胞活力下降和凋亡(P<0.05),显著升高了LC3II/LC3I比值以及Beclin1、Parkin和Pink1表达水平(P<0.05)。结论 比索洛尔可能通过Drp1/Parkin/Pink1通路激活线粒体自噬,减少心肌细胞凋亡来保护心肌细胞缺氧/复氧损伤。Objective Mitochondrial autophagy plays an important role in myocardial ischemia/reperfusion injury. We investigated whether bisoprolol protects myocardial ischemia/reperfusion(I/R) injury through Drp1/Pink1/Parkin pathway. Methods We used a hypoxia/reoxygenation cell model, H9c2 cells were treated with 6 hours of hypoxia followed by 12 hours of reoxygenation. The experiment was divided into four groups: control;hypoxia/reoxygenation;hypoxia/reoxygenation+bisoprolol;bisoprolol. Lentiviral vector with low Drp1 expression(Drp1-siRNA) was established to measure the cell viability, apoptosis, mitochondrial fission and autophagy. Results After the establishment of the hypoxia/reoxygenation cell model, and after the treatment with bisoprolol, the cell survival rate increased to 83.25% ±2.3%(P<0.05);the apoptosis rate decreased by 30%(P<0.05);bisoprolol could also reduce the expression of Drp1(P<0.05) and increase the expression of LC3, Beclin1, Pink1 and Parkin(P<0.05). The results of the Drp1-siRNA assay showed that compared with scramble treatment, Drp1-siRNA treatment reduced the decrease of viability and apoptosis of H9c2 cells induced by hypoxia/reoxygenation(P<0.05), and significantly increased the ratio of LC3II/LC3I and the expression of Beclin1, Parkin and Pink1(P<0.05). Conclusion Bisoprolol may protect myocardial cells from hypoxia/reoxygenation injury by activating mitochondrial autophagy and reducing myocardial cell apoptosis through Drp1/Parkin/Pink1 pathway.
关 键 词:比索洛尔 缺氧/复氧 H9C2细胞 线粒体自噬 线粒体分裂 心肌细胞
分 类 号:R542.2[医药卫生—心血管疾病]
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