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蟾毒灵对低氧/复氧心肌细胞损伤保护作用及机制 被引量:1

PROTECTIVE EFFECT OF BUFALIN AGAINST HYPOXIA/REOXYGENATION-INDUCED MYOCARDIAL INJURY AND RELA-TED MECHANISM
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摘要 目的研究蟾毒灵对低氧/复氧(H/R)心肌细胞损伤的影响,并初步探究其作用机制。方法体外建立H/R心肌细胞模型,并采用不同浓度(0.1、1.0、10.0μmol/L)的蟾毒灵处理。采用CCK-8法测定细胞活力,酶标法检测超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,流式细胞术检测心肌细胞凋亡率和活性氧(ROS)水平,Western blot检测剪切的含半胱氨酸的天冬氨酸蛋白水解酶3和9(Cleaved Caspase-3,Cleaved Caspase-9)蛋白水平。结果与空白对照组比较,H/R组心肌细胞活力、SOD含量明显降低,ROS水平、MDA含量、细胞凋亡率、Cleaved Caspase-3和Cleaved Caspase-9蛋白表达升高(F=129.978~330.050,P<0.05)。蟾毒灵可明显改善H/R引起的上述指标变化。结论蟾毒灵能够改善H/R引起的心肌细胞损伤,其作用机制可能与抑制氧化应激和细胞凋亡有关。 Objective To investigate the effect of bufalin on hypoxia/reoxygenation(H/R)-induced cardiomyocyte injury and its mechanism of action.Methods An H/R cardiomyocyte model was established in vitro and cardiomyocytes were treated with bufalin at different concentrations(0.1,1.0,and 10.0μmol/L).CCK-8 assay was used to determine cell viability;ELISA was used to measure the content of superoxide dismutase(SOD)and malondialdehyde(MDA);flow cytometry was used to measure cardiomyocyte apoptosis and reactive oxygen species(ROS)level;Western blot was used to measure the levels of cleaved cysteine-containing aspartate proteolytic enzymes 3 and 9(cleaved caspase-3 and cleaved caspase-9).Results Compared with the blank control group,the H/R group had significant reductions in cardiomyocyte viability and SOD content and significant increases in ROS level,MDA content,apoptosis rate,and protein expression of cleaved caspase-3 and cleaved caspase-9(F=129.978-330.050,P<0.05).Bufalin significantly improved the above changes in these indices caused by H/R.Conclusion Bufalin can improve cardiomyocyte injury caused by H/R,possibly by inhibiting oxidative stress and cell apoptosis.
作者 翟小菊 李松林 马光 王国良 惠学志 ZHAI Xiaoju;LI Songlin;MA Guang;WANG Guoliang;HUI Xuezhi(Department of Cardiology,The First Affiliated Hospital of Henan University,Kaifeng 475000,China)
出处 《青岛大学学报(医学版)》 CAS 2021年第1期115-119,共5页 Journal of Qingdao University(Medical Sciences)
基金 河南省医学科技攻关计划项目(2018020314)。
关键词 蟾酥碱 肌细胞 心脏 心肌再灌注损伤 活性氧 细胞凋亡 Bufotenin myocytes,cardiac myocardial reperfusion injury reactive oxygen species apoptosis
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