氧化应激对原代培养乳鼠心房肌细胞中内质网应激及凋亡因子的影响  

Effect of oxidative stress on myocardial apoptosis,endoplasmic reticulum stress and apoptosis factor in suckling mouse atria myocardium

作　　者：龙杰[1] 王羽[1] 刘晓翠[1] 于淼[1] 王伊林[1] 黄侠[1] 赵明[2] 

机构地区：[1]内蒙古民族大学,通辽028000 [2]内蒙古民族大学附属医院,通辽028000

出　　处：《中国应用生理学杂志》2017年第2期185-188,共4页Chinese Journal of Applied Physiology

摘　　要：目的:研究氧化应激对原代培养乳鼠心房肌细胞凋亡、内质网应激及凋亡因子的影响。方法:实验分2组:对照组、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2 h,检测氧化和抗氧化指标超氧化物歧化酶(SOD)活力、丙二醛(MDA)及还原型谷胱甘肽(GSH)含量;检测细胞凋亡、细胞GRP78、GRP94及chop、bax、bcl-2 m RNA表达。结果:与对照组相比较,氧化应激组心房肌细胞SOD活力和GSH含量下降、MDA含量增加(P<0.01),细胞凋亡增加(P<0.01),细胞GRP78、GRP94、chop、bax m RNA表达增加、bcl-2 m RNA表达减少(P<0.01)。结论:氧化应激反应可能介导内质网应激反应并激活促凋亡因子表达,抑制抗凋亡因子表达,引起心房肌细胞凋亡增加。这可能与心房纤颤的发生有一定关联性。Objective： To investigate the relationship between oxidative stress and myocardial apoptosis, endoplasmic reticulum stress, apoptosis-inducing factors in the process of by researching the effect of oxidative stress on myocardial apoptosis, endoplasmic reticalum stress and apoptosis factor--chop, bax, bcl-2 in suckling mouse atria myocardium. Methods： The primary cultured suckling mouse myocardium were randomly divided into control group and oxidative stress group. Firstly, the suckling mouse atria cardiomyocytes were treated with H2O2 at the concentration of 100 m μmol/L for 2 hours. Then, the index of oxidative stress and anti-oxidative stress superoxide dismutase （SOD）, the contents of malondialdehyde （MDA） and glutathione （GSH） of this two groups were detected by ELISA. Myocardial apoptosis of the two groups was detected by TUNEL. The expressions of glucose-regulated protein 78 （GRP78）, glucose-regulated protein 94 （GRP94）, C/EBP homolo- gous protein （chop）, Bcl-2 associated X protein （bax）, B-cell leukemia 2 protein （bcl-2） mRNA were detected by real time PCR. Results： Compared with the control group, the viability of SOD and the contents of MDA in oxidative stress group were reduced, the contents of MDA was increased （ P 〈 0.01）. Compared with the control group, the expression of myocardial apoptosis in oxidative stress group was increased（ P 〈 0.01 ） ; the expressions of GRP78, GRP94, chop and bax mRNA were increased, while the expression of bcl-2 mRNA was reduced in oxidative stress group. Conclusion： Oxidative stress may induce the endoplasmic reticulum stress, activate the expressions of apoptosis factors, and finally increase the myocardial apoptosis of atria cardiomyocytes. This may connected to the incident of atrial fibrillation.

关 键 词：氧化应激 内质网应激 凋亡 心房纤颤 

分 类 号：R331.3[医药卫生—人体生理学] R-332[医药卫生—基础医学]