吡咯二硫氨基甲酸酯对缺氧复氧诱导的心肌细胞凋亡和细胞焦亡的影响  

Effects of pyrrolidine dithiocarbamate on cardiomyocyte apoptosis and apoptosis ynduced by anoxia and reoxygenation

作　　者：韩敏 董佳佳 刘帅[1] 马依彤[2] HAN Min;DONG Jiajia;LIU Shuai;MA Yitong(The First Clinical Medical College and the First Affiliated Hospital,Urumqi 830054,China;Department of Cardiology,First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,China)

机构地区：[1]新疆医科大学第一临床医学院暨第一附属医院,乌鲁木齐830054 [2]新疆医科大学第一附属医院心脏中心,乌鲁木齐830054

出　　处：《新疆医科大学学报》2020年第2期125-130,共6页Journal of Xinjiang Medical University

基　　金：国家自然科学基金(81873490);新疆维吾尔自治区研究生科研创新计划项目(XJ2019G183);新疆医科大学研究生创新创业项目(CXCY2018020)

摘　　要：目的探讨吡咯二硫氨基甲酸酯(Pyrrolidinedithiocarbamate,PDTC)对心肌缺血再灌注损伤的保护作用。方法建立缺氧/复氧(Hypoxia/Reoxygenation,H/R)模型,测定心肌细胞活力及乳酸脱氢酶(LDH)水平。Hoechst/PI和流式细胞仪法检测心肌细胞凋亡及焦亡比例;免疫印迹法检测心肌细胞NF-κB核转位以及细胞凋亡、焦亡蛋白的表达。结果与正常组相比,H/R组细胞活力下降,LDH升高,NF-κB入核、Bax/Bcl-2、GSDMD、IL-1β表达增加,细胞凋亡及焦亡比例增加,而PDTC可逆转上述结果,差异有统计学意义(P<0.05)。结论PDTC能有效抑制缺氧复氧诱导的NF-κB活化、心肌细胞凋亡及细胞焦亡,从而改善心肌缺血再灌注损伤。Objective To explore the protective effect of PDTC on myocardial ischemia-reperfusion injury(MIRI).Methods Hypoxia/reoxygenation(H/R)model was established,and cell damage was assessed using CCK8 and LDH assays.Hoechst/PI and flow cytometry were used to detect cell apoptosis and pyroptosis;Western blotting was used to detect the nuclear translocation of p65 and the expression of apoptosis and pyroptosis-related proteins.Results Compared with the normal group,the cell viability of the H/R group decreased,NF-κB translocation,LDH level,apoptotic and pyroptic rates,Bax/Bcl-2,GSDMD,IL-1βexpression increased,but PDTC improved the cell viability and attenuated LDH level and the proportion of cell death.Moreover,the NF-κB nuclear translocation and the expressions of Bax/Bcl-2,GSDMD,and IL-1βwere significantly inhibited by PDTC(P<0.05).Conclusion PDTC effectively reduced MIRI through inhibiting NF-κB activation,apoptosis and pyroptosis.

关 键 词：NF-ΚB 细胞凋亡 细胞焦亡 心肌缺血再灌注损伤 

分 类 号：R542.2[医药卫生—心血管疾病]