[1]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):551-555.[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,(04):551-555.[doi:10.13705/j.issn.1671-6825.2019.01.121]
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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()
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《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2019年04期
页码:
551-555
栏目:
应用研究
出版日期:
2019-07-20

文章信息/Info

Title:
Effects of KLF11 overexpression on viability and oxidative stress of H9c2 cardiomyocytes induced by H2O2
作者:
王 滨1)王文华2)辛传友1)郭龙哲1)黄传奇1)郜 阳3)宁文龙1)
1)齐齐哈尔市第一医院急诊内科 黑龙江齐齐哈尔 161000;2)齐齐哈尔市第一医院风湿科 黑龙江齐齐哈尔 161000;3)哈尔滨医科大学附属第二医院重症医学科 哈尔滨 150000
Author(s):
WANG Bin1)WANG Wenhua2)XIN Chuanyou1)GUO Longzhe1)HUANG Chuanqi1)GAO Yang3)NING Wenlong1)
1)Emergency Department of Internal Medicine, Qiqihar First Hospital,Qiqihar,Heilongjiang 161000;2)Department of Rheumatology,Qiqihar First Hospital, Qiqihar,Heilongjiang 161000;3)Department of Critical Care Medicine, the Second Affiliated Hospital,Ha'erbin Medical University, Ha'erbin, Heilongjiang 150000
关键词:
心肌细胞 KLF11基因 凋亡 PI3K/AKT信号通路 氧化应激
Keywords:
cardiomyocyte KLF11 gene apoptosis PI3K/AKT signaling pathway oxidative stress
分类号:
R541
DOI:
10.13705/j.issn.1671-6825.2019.01.121
摘要:
目的:探讨KLF11过表达对H2O2诱导的H9c2心肌细胞活力和氧化应激水平的影响及机制。方法:将H9c2细胞分为空白组、H2O2组、空质粒+H2O2组和KLF11+H2O2组。H2O2组使用200 μmol/L的H2O2处理细胞6 h。空质粒+H2O2组和KLF11+H2O2组细胞分别转染pcDNA3.1及pcDNA3.1-KLF11 48 h后,使用200 μmol/L H2O2处理6 h。MTT法检测4组细胞活力,Annexin V-FITC/PI双染法检测细胞凋亡率,采用SOD及MDA检测试剂盒检测细胞中SOD活力及MDA含量,Western blot法检测细胞中PI3K、p-AKT和Bcl-2蛋白表达水平。结果:与空白组比较,H2O2组H9c2细胞活力降低,凋亡率增加; 细胞中SOD活力降低, MDA含量增加; 同时PI3K、p-AKT和Bcl-2蛋白表达下调(P<0.05)。与H2O2组比较,KLF11+H2O2组细胞活力增强,凋亡率降低; 细胞中SOD活力增加,MDA含量降低; 同时PI3K、p-AKT和Bcl-2蛋白表达上调(P<0.05)。结论:KLF11可能通过激活PI3K/AKT信号通路,抑制氧化应激,提高H2O2诱导的H9c2细胞的活力。
Abstract:
Aim:To investigate the effects of KLF11 overexpression on the viability and oxidative stress of H9c2 cardiomyocytes induced by H2O2 and its mechanism.Methods:H9c2 cells were allocated into blank group, H2O2 group, pcDNA3.1+H2O2 group and pcDNA3.1-KLF11+H2O2 group. The cells in H2O2 group were treated with 200 μmol/L H2O2 for 6 hours. The latter two groups were transfected with pcDNA3.1 or pcDNA3.1-KLF11 for 48 hours,respectively, and then treated with H2O2 for 6 hours. Cell viability and apoptotic rate were detected by MTT and Annexin V-FITC/PI staining, SOD activity and MDA content in the cells were detected, and the expressions of PI3K, p-AKT and Bcl-2 proteins were detected by Western blot.Results:Compared with those of the blank group, the viability of cells in H2O2 group was inhibited; apoptosis was induced, SOD activity was reduced, MDA content was increased; and the expressions of PI3K, p-AKT and Bcl-2 proteins were down-regulated significantly(P<0.05).While compared with those of the H2O2 group, the viability of cells in pcDNA3.1-KLF11+H2O2 group was induced, apoptosis was inhibited; SOD activity was increased, MDA content was decreased; and the expressions of PI3K, p-AKT and Bcl-2 proteins were up-regulated significantly(P<0.05).Conclusion:KLF11 can improve H9c2 cell viability interfered by H2O2, which may be related to the inhibition of oxidative stress and activation of PI3K/AKT signaling pathway.

参考文献/References:

[1] HARMON JS,STEIN R,ROBERTSON RP.Oxidative stress-mediated,post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells[J].J Biol Chem,2016,280(12):11107
[2] WRAY DW,AMANN M,RICHARDSON RS.Peripheral vascular function,oxygen delivery and utilization:the impact of oxidative stress in aging and heart failure with reduced ejection fraction[J].Heart Fail Rev,2016,22(2):1
[3] YU HJ,GUAN QG,GUO L,et al.Gypenosides alleviate myocardial ischemia-reperfusion injury via attenuation of oxidative stress and preservation of mitochondrial function in rat heart[J].Cell Stress Chaperones,2016,21(3):429
[4] HABENER A,CHOWDHURY A,ECHTERMEYER FA,et al.MitoNEET Protects HL-1 Cardiomyocytes from Oxidative Stress Mediated Apoptosis in an In Vitro Model of Hypoxia and Reoxygenation[J].PLoS One,2016,11(5):e0156054
[5] TANG XE,LIU K,HAMBLIN MH,et al.Genetic Deletion of Kruppel-like factor 11 aggravates ischemic brain injury[J].Mol Neurobiol,2018,55(4):2911
[6] ZHENG Y,KONG Y,LI F.Kruppel-like transcription factor 11(KLF11)overexpression inhibits cardiac hypertrophy and fibrosis in mice[J].Biochem Biophys Res Commun,2014,443(2):683
[7] ASENSIO-LOPEZ MC,SOLER F,PASCUAL-FIGAL D,et al.Doxorubicin-induced oxidative stress:the protective effect of nicorandil on HL-1 cardiomyocytes[J].PLoS One,2017,12(2):e0172803
[8] YANG YC,TSAI CY,CHEN CL,et al.Pkc delta activation is involved in ros-mediated mitochondrial dysfunction and apoptosis in cardiomyocytes exposed to advanced glycation end products(ages)[J].Aging Dis,2018,9(4):647
[9] WEI C,LI L,KIM IK,et al.NF-κB mediated miR-21 regulation in cardiomyocytes apoptosis under oxidative stress[J].Free Radic Res,2014,48(3):282
[10]吕品.microRNA-24调控H2O2诱导的H9c2心肌细胞凋亡的实验研究[D].郑州:郑州大学,2014.
[11]YIN KJ,FAN YB,HAMBLIN M,et al.KLF11 mediates PPAR gamma cerebrovascular protection in ischaemic stroke[J].Brain,2013,136(4):1274
[12]胡梦竹,王娟,王盼盼,等.RNA干扰人永生化食管上皮恶变细胞中核干细胞因子对PI3K/AKT表达的影响[J].郑州大学学报(医学版),2016,51(6):700
[13]DEY JH,BIANCHI F,VOSHOL J,et al.Targeting fibroblast growth factor receptors blocks PI3K/AKT signaling, induces apoptosis, and impairs mammary tumor outgrowth and metastasis[J].Cancer Res,2010,70(10):4151
[14]YU W,ZHA WL,KE ZQ,et al.Curcumin protects neonatal rat cardiomyocytes against high glucose-induced apoptosis via PI3K/Akt signalling pathway[J].J Diabetes Res,2016(23):1
[15]WANG JY,CHEN H,ZHOU Y,et al.Atorvastatin inhibits myocardial apoptosis in a swine model of coronary microembolization by regulating PTEN/PI3K/Akt signaling pathway[J].Cell Physiol Biochem,2016,38(1):207

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备注/Memo

备注/Memo:
【基金项目】黑龙江省卫生和计划生育委员会科技计划项目(2016-049)
【作者简介】宁文龙,通信作者,男,1964年9月生,硕士,主任医师,研究方向:急诊急救,E-mail:dipomi6843093@163.com
更新日期/Last Update: 2019-07-20