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同型半胱氨酸经PERK磷酸化激活CHOP-ERO1α通路介导心肌细胞凋亡的研究
引用本文:杜海林,杨绍兵,丛广志,王凯,贾绍斌.同型半胱氨酸经PERK磷酸化激活CHOP-ERO1α通路介导心肌细胞凋亡的研究[J].重庆医学,2018(5):584-587.
作者姓名:杜海林  杨绍兵  丛广志  王凯  贾绍斌
作者单位:宁夏医科大学临床医学院,银川,750004 宁夏医科大学总医院心脏中心,银川,750004
基金项目:国家自然科学基金资助项目
摘    要:目的 探讨同型半胱氨酸(Hcy)对心肌的损伤作用及其可能机制.方法 选用H9C2心肌细胞,分别用不同浓度Hcy、4-苯基丁酸(4-PBA)干预细胞.将H9C2细胞分为对照组、H400组、H400P2组,对照组使用普通培养基,H400组加入400μmol/L的Hcy,H400P2组在H400组基础上加入2 mmol/L的4-PBA.CCK-8检测细胞存活率,TUNEL染色评估细胞凋亡,免疫细胞化学检测内质网氧化还原酶1α(ERO1α)表达,Western blot检测蛋白表达差异.结果 Hcy对H9C2心肌细胞损伤呈浓度依赖性(F=2 039.958,P<0.01).与对照组比较,H400组细胞凋亡分数及胰腺内质网激酶(PERK)、磷酸化PEPK(p-PERK)、CCAAT增强子结合蛋白同源蛋白(CHOP)、ERO1α表达均增加(P<0.01);H400P2组细胞凋亡分数及PERK、p-PERK、CHOP、ERO1α表达均有所下降,与H400组比较均差异有统计学意义(P<0.05).结论 Hcy通过内质网应激机制介导心肌细胞凋亡.

关 键 词:同型半胱氨酸  CCAAT增强子结合蛋白同源蛋白  内质网氧化还原酶a  肌细胞  心脏  细胞凋亡  homocysteine  CCAAT-enhancer-binding  protein  homologous  protein  endoplasmic  reticulum  oxidoreductin-α  myocytes  cardiac  apoptosis

Homocysteine mediates cardiomyocyte apoptosis by phosphorylating PERK and activating CHOP-ERO1α pathway
DU Hailin,YANG Shaobing,CONG Guangzhi,WANG Kai,JIA Shaobin.Homocysteine mediates cardiomyocyte apoptosis by phosphorylating PERK and activating CHOP-ERO1α pathway[J].Chongqing Medical Journal,2018(5):584-587.
Authors:DU Hailin  YANG Shaobing  CONG Guangzhi  WANG Kai  JIA Shaobin
Abstract:Objective To investigate the effects of homocysteine(Hcy) on myocardial injury and its possible mechanisms.Methods The selected H9C2 cardiomyocytes were intervened with various concentrations of Hcy and 4-phenyl butyric acid(4-PBA).The H9C2 cells were divided into the control group,H400 group and H400P2 group.The control group used the common medium,the H400 group was added with 400 μmol/L Hcy,the H400P2 group was added with 2 mmol/L 4-PBBA on the basis of H400 group.The cell livability was detected by using cell counting kit-8 (CCK-8).Apoptosis was evaluated by using the terminal deoxynucleotidyl transferase mediated nick-end labelling(TUNEL) staining.The ERO1α expression was determined by using immunocytochemistry,and the protein expression difference was determined by using Western blot.Results The injury of Hey on H9C2 cardiomyocytes showed a concentration-dependent manner(F=2 039.958,P<0.01).Compared with the control group,the apoptosis percentages and expression levels of PERK,p-PERK,CHOP and ERO1α in the H400 group were increased(P<0.01);while which in the H400P2 group were decreased,the difference was statistically significant(P<0.05).Conclusion Hcy mediates myocardial apoptosis through endoplasmic reticulum stress mechanism.
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