[1]张 杰),刘 亮),周 辉),等.上调抗增殖蛋白表达对TNF-α诱导的H9c2心肌细胞损伤的影响[J].郑州大学学报(医学版),2019,(05):728-732.[doi:10.13705/j.issn.1671-6825.2018.07.011]
 ZHANG Jie),LIU Liang),ZHOU Hui),et al.Effects of up-regulation of anti-proliferative protein expression on TNF-α induced cardiomyocyte injury[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(05):728-732.[doi:10.13705/j.issn.1671-6825.2018.07.011]
点击复制

上调抗增殖蛋白表达对TNF-α诱导的H9c2心肌细胞损伤的影响()
分享到:

《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2019年05期
页码:
728-732
栏目:
应用研究
出版日期:
2019-09-20

文章信息/Info

Title:
Effects of up-regulation of anti-proliferative protein expression on TNF-α induced cardiomyocyte injury
作者:
张 杰1)刘 亮1)周 辉1)郭桂喜1)于 强1)银鹏飞2)陈文强3苏 兴3)
1)北大医疗鲁中医院心血管内科 山东淄博 255400;2)北京大学国际医院心内科 北京102200;3)山东大学齐鲁医院心内科 济南 250012
Author(s):
ZHANG Jie1) LIU Liang1) ZHOU Hui1)GUO Guixi1)YU Qiang1)YIN Pengfei2) CHEN Wenqiang3)SU Xing3)
1)Department of Cardiovascular Medicine,Luzhong Hospital, Peking University Medical Center, Zibo, Shandong 255400;2)Department of Cardiology, International Hospital of Peking University, Beijing, 102200;3)Department of Cardiology,Qilu Hospital,Shandong Un
关键词:
心肌细胞 抗增殖蛋白 TNF-α 细胞损伤 H9c2细胞
Keywords:
cardiomyocyte prohibitin TNF-α cell injury H9c2 cell
分类号:
R542.2
DOI:
10.13705/j.issn.1671-6825.2018.07.011
摘要:
目的:研究抗增殖蛋白(PHB)在肿瘤坏死因子-α(TNF-α)诱导的心肌细胞损伤中的作用。方法:将心肌H9c2细胞分为4组,以不感染病毒且不用TNF-α处理的H9c2细胞作为对照组,以不感染病毒、仅用20 μg/L的TNF-α细胞培养液培养的细胞作为TNF-α组,以行Lv-PHB或Lv-NC感染、并用含有20 μg/L的TNF-α细胞培养液培养24 h的细胞作为Lv-PHB+TNF-α组和Lv-NC+TNF-α组。采用MTT法测定4组细胞的增殖活性,比色法检测细胞乳酸脱氢酶(LDH)漏出率,双染法检测细胞凋亡,Western blot检测细胞中Cleaved Caspase-3、CCAAT/增强子结合蛋白同源蛋白(CHOP)、Cleaved Caspase-12蛋白表达水平。结果:Lv-PHB+TNF-α组细胞中PHB蛋白和mRNA表达水平高于TNF-α组(P<0.05)。与对照组比较,TNF-α组细胞增殖活性降低,LDH漏出率升高,凋亡率升高,细胞中Cleaved Caspase-3、CHOP、Cleaved Caspase-12蛋白水平也升高(P<0.05)。与TNF-α组比较,Lv-PHB+TNF-α组细胞增殖活性升高,LDH漏出率降低,凋亡率降低,细胞中Cleaved Caspase-3、CHOP、Cleaved Caspase-12蛋白水平降低(P<0.05)。结论:上调PHB表达可以减轻TNF-α诱导的心肌细胞损伤,提高心肌细胞活性、降低细胞凋亡水平。
Abstract:
Aim:To study the role of prohibitin(PHB)in TNF-α induced cardiomyocyte injury.Methods:H9c2 myocardial cells were divided into 4 groups:control group(not treated),TNF-α group(treated by 20 μg/L TNF-α for 24 h),Lv-PHB+TNF-α group(infected by Lv-PHB and treated by 20 μg/L TNF-α),Lv-NC+TNF-α group(infected by Lv-NC and treated by 20 μg/L TNF-α). The proliferation activity was determined by MTT method, the leakage rate of lactate dehydrogenase(LDH)was detected by colorimetry, the apoptosis was detected by double staining, and the levels of Cleaved Caspase-3, CCAAT/enhancer binding protein(CHOP), and activated Caspase-12 were detected by Western blot.Results:Compared with the control group,the level of PHB protein and mRNA in H9c2 cells of TNF-α group increased, the proliferation activity of TNF-α group decreased, the leakage rate of LDH increased, the rate of apoptosis increased,and the levels of Cleaved Caspase-3, CHOP and Cleaved Caspase-12 protein also increased in cells(P<0.05).Compared with TNF-α group, cell proliferation activity increased, the leakage rate of LDH was reduced, the rate of apoptosis was decreased, and the level of Cleaved Caspase-3, CHOP and Cleaved Caspase-12 protein decreased in Lv-PHB+TNF-α group(P<0.05).Conclusion:Up-regulation of PHB can alleviate TNF-α induced myocardial cell injury, improve the activity of myocardial cells and reduce the level of apoptosis.

参考文献/References:

[1] DU H,HAO J,LIU F,et al.Apigenin attenuates acute myocardial infarction of rats via the inhibitions of matrix metalloprotease-9 and inflammatory reactions[J].Int J Clin Exp Med,2015,8(6):8854
[2] PARAPANOV R,LUGRIN J,ROSENBLATT-VELIN NA,et al.Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse[J].Clin Sci,2015,129(2):187
[3] WU HX,WANG GN,LI S,et al.TNF-αMediated-p38-dependent signaling pathway contributes to myocyte apoptosis in rats subjected to surgical trauma[J].Cell Physiol Biochem,2015,35(4):1454
[4] 徐旭,李志伟,郭雅琼,等.重症颅脑损伤后 TNF-α及 IL-6在急性心肌功能损害中的作用[J]〗.重庆医学,2015,44(6):793
[5] 刘翠云.miR-361/PHB1通路对心脏缺血损伤的调控作用[D].北京:中国科学院大学,2015
[6] 李蕊. PHB对高糖环境下的心肌细胞中活性氧及细胞凋亡的影响及机制研究[J]. 中国免疫学杂志, 2017, 33(12):1789
[7] 赵雪峰,魏秀华.血浆BNP、TNF-α、sTWEAK水平变化与心力衰竭的相关性分析[J].中国实验诊断学,2018,22(5):31
[8] 刘媛媛,田学峰,霍红,等.心肌缺血再灌注损伤患者血清TNF-α和IL-10水平变化及意义[J].中国医学前沿杂志:电子版,2018,10(1):79
[9] 江海宙,苏兰利.TNF-α与常见血管类疾病的关系[J].健康研究,2018, 38(5):54
[10]毛洪雅,季永.抗增殖蛋白与心肌保护[J].国际麻醉学与复苏杂志,2015,36(1):88
[11]毛洪雅,杨洁琼,季永.JAK2/STAT3调节抗增殖蛋白表达在 H2S后处理心肌细胞中的保护作用[J].中国药理学通报,2014,30(8):1122
[12]WANG GJ,GUO LY,WANG HX,et al.IP3R and RyR calcium channels are involved in neonatal rat cardiac myocyte hypertrophy induced by tumor necrosis factor-α[J].Am J Transl Res,2017,9(2):343
[13]HU Hai, TIAN MX, DING C,et al.The C/EBP homologous protein(CHOP)transcription factor functions in endoplasmic reticulum stress-induced apoptosis and microbial infection[J].Frontiers Immunol,2019,9:3083
[14]HETZ C,RUSSELAKIS-CARNEIRO M,MAUNDRELL K,et al.Caspase-12 and endoplasmic reticulum stress mediate neurotoxicity of pathological prion protein[J].EMBO J,2003,22(20):5435
[15]CHEN Y,TANG Y,XIANG Y,et al.Shengmai injection improved doxorubicin-induced cardiomyopathy by alleviating myocardial endoplasmic reticulum stress and Caspase-12 dependent apoptosis[J].Biomed Res Int, 2015. doi: 10.1155/2015/952671

相似文献/References:

[1]赵杰)△,薛文华),梁淑红).香青兰提取物对体外培养乳鼠心肌细胞缺氧/复氧损伤的保护作用[J].郑州大学学报(医学版),2010,(03):485.
 ZHAO Jie),XUE Wenhua),LIANG Shuhong).Protective effects of dracocephalum moldavica extracts on hypoxia/reoxygenation injury of cardiomyocytes in cultured neonatal rat[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2010,(05):485.
[2]罗萍)△,杜松),段红艳),等.普罗布考对过氧化氢诱导的大鼠心肌细胞凋亡及氧化应激水平的影响*[J].郑州大学学报(医学版),2011,(06):846.
 LUO Ping),DU Song),DUAN Hongyan),et al.Inhibition of probucol on cultured neonatal rat cardiomyocyte apoptosis induced by hydrogen peroxide[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2011,(05):846.
[3]郭文静),樊红琨),郑春光),等.沉默JP2基因对小鼠心肌细胞SK2通道的影响*[J].郑州大学学报(医学版),2015,(01):55.
 GUO Wenjing),FAN Hongkun),ZHENG Chunguang),et al.Effects of targeting JP2 RNAi on SK2 channel in mouse cardiomyocytes[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2015,(05):55.
[4]王 滨),王文华),辛传友),等.KLF11过表达对H2O2诱导的H9c2心肌细胞活力及氧化应激水平的影响[J].郑州大学学报(医学版),2019,(04):551.[doi:10.13705/j.issn.1671-6825.2019.01.121]
 WANG Bin),WANG Wenhua),XIN Chuanyou),et al.Effects of KLF11 overexpression on viability and oxidative stress of H9c2 cardiomyocytes induced by H2O2[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(05):551.[doi:10.13705/j.issn.1671-6825.2019.01.121]
[5]张思洁,吴亚琼,李星涛.p38MAPK抑制剂联合辅酶Q10对氧化应激条件下大鼠心肌细胞的保护作用[J].郑州大学学报(医学版),2019,(05):699.[doi:10.13705/j.issn.1671-6825.2018.09.057]
 ZHANG Sijie,WU Yaqiong,LI Xingtao.Protective effects of p38MAPK inhibitor combined with coenzyme Q10 on myocardial cells under oxidative stress[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(05):699.[doi:10.13705/j.issn.1671-6825.2018.09.057]

备注/Memo

备注/Memo:
【基金项目】山东省自然科学基金项目(ZR2015HL130)
【作者简介】张杰,男,1969年11月生,本科,副主任医师,研究方向:冠心病、心绞痛、心肌梗死等疾病的诊治,E-mail:715314153@qq.com
更新日期/Last Update: 2019-09-20