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氧化应激对乳鼠心肌细胞网腔钙结合蛋白、内质网应激及信号传导通路作用的研究 被引量:6

Effects of oxidative stress on the expression of calumenin,endoplasmic reticulum stress and signal transduction pathway in suckling mouse atrial myocytes
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摘要 目的:研究氧化应激对原代培养乳鼠心房肌细胞网腔钙结合蛋白(calumenin)、内质网应激及信号传导通路作用,探讨氧化应激与心房肌细胞网腔钙结合蛋白、内质网应激及其凋亡信号传导通路相关性。方法:实验分2组:对照组和氧化应激组。原代培养乳鼠心房肌细胞,氧化应激组在培养的原代心房肌细胞中加入终浓度为100μmol/L的H2O2培养2h,检测氧化和抗氧化指标的变化。ELASE法检测2组心房肌细胞超氧化物歧化酶(SOD)活力、丙二醛(MDA)及还原型谷胱甘肽(GSH)含量。Western bloting检测2组心房肌细胞GRP78、GRP94、chop、IRE1及caspase-3、caspase-9、caspase-12表达。结果:1与对照组比较,氧化应激组心房肌细胞SOD活力下降,GSH含量下降,MDA含量增加(P<0.01)。2与对照组比较,氧化应激组心房肌细胞calumenin表达减少(P<0.01),而GRP78、GRP94、chop、IRE1及caspase-3、caspase-9、caspase-12表达增加(P<0.01)。结论:氧化应激反应能引起心房肌细胞calumenin表达减少,这可能介导心房肌细胞内质网应激反应并激活其凋亡信号传导通路表达,导致心房肌细胞凋亡,参与心房结构重构引发房颤。 Objective:To investigate the effect of oxidative stress on the expression of calumenin,endoplasmic reticulum stress and signal transduction pathway in the primary cultured suckling mouse atrial myocytes,and to explore the correlation between oxidative stress and the expression of calumenin,endoplasmic reticulum stress and apoptosis signal transduction pathway.Method:The suckling mouse myocardium of primary culture were randomly divided into control group and the oxidative stress group.Each group was cultured 2hwith the concentration of100umol/L H2O2,then detected the changes of oxidation and antioxidation indexs.The activity of superoxide dismutase(SOD)and the content of malondialdehyde(MDA)and glutathione(GSH)in 2groups were detected by ELASE assay.The expression of GRP78,chop,IRE1,Caspase-3,caspase-12,GRP94 and caspase-9were detected by Western bloting.Result:Compared with the control group,the SOD activity and the GSH content of the atrial myocytes in the oxidative stress group were decreased,and the content of MDA was increased(P〈0.01).Compared with the control group,the expression of calumenin was decreased in the oxidative stress group(P〈0.01),while the expression of GRP94,chop,IRE1 and Caspase-3,caspase-9,GRP78,and caspase-12 were increased.Conclusion:Oxidative stress can induce the expression of calumenin in atrial myocytes,which may mediate the endoplasmic reticulum stress reaction and activate the expression of the apoptosis signal transduction pathway.This leads to the apoptosis of atrial myocytes and involves in atrial structural remodeling of atrial fibrillation.
出处 《临床心血管病杂志》 CAS CSCD 北大核心 2016年第6期611-613,共3页 Journal of Clinical Cardiology
关键词 氧化应激 网腔钙结合蛋白 内质网应激 凋亡 oxidative stress calumenin endoplasmic reticulum stress apoptosis
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  • 1周自强,胡大一,陈捷,张仁汉,李奎宝,赵秀丽.中国心房颤动现状的流行病学研究[J].中华内科杂志,2004,43(7):491-494. 被引量:1402
  • 2姚丽梅,陈宇明,尹瑞兴.生长激素对大鼠阿霉素性心肌病心肌细胞凋亡的影响[J].基础医学与临床,2005,25(8):742-745. 被引量:9
  • 3姚丽梅,陈宇明,尹瑞兴.生长激素对大鼠阿霉素心肌病心肌细胞凋亡及Fas的影响[J].广西医科大学学报,2005,22(4):509-511. 被引量:4
  • 4Lozano HF,Conde CA,Florin T,et al.Treatment and prevention of atrial fibrillation with non-antiarrhythmic pharmacologic therapy[J].Heart Rhythm,2005,2 (9):1000-1007. 被引量:1
  • 5Shiroshita-Takeshita A,Schram G,Lavoie J,et al.Effect of simvastatin and antioxidant vitamins on atrial fibrillation promotion by atrial-tachycardia remodeling in dogs[J].Circulation,2004,110 (16):2313-2319. 被引量:1
  • 6Caouette D,Dongmo C,B(e)rub(e) J,et al.Hydrogen peroxide modulates the Kv1.5 channel expressed in a mammalian cell line[J].Naunyn Schmiedebergs Arch Pharmacol,2003,368 (6):479-486. 被引量:1
  • 7Fearon IM,Palmer AC,Balmforth AJ,et al.Hypoxic and redox inhibition of the human cardiac L-type Ca2+ channel[J].Adv Exp Med Biol,2000,475:209-218. 被引量:1
  • 8Mihm MJ,Yu F,Carnes CA,et al.Impaired myofibrillar energetics and oxidative injury during human atrial fibrillation[J].Circulation,2001,104(2):174-180. 被引量:1
  • 9Rude MK,Duhaney TA,Kuster GM,et al.Aldosterone stimulates matrix metalloproteinases and reactive oxygen species in adult rat ventricular cardiomyocytes[J].Hypertension,2005,46(3):555-561. 被引量:1
  • 10Goette A,Arndt M,Rocken C,et al.Calpains and cytokines in fibrillating human atria[J].Am J Physiol Heart Circ Physiol,2002,283 (1):H264-H272. 被引量:1

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