AE3通过NO通路参与心肌细胞缺氧预适应的保护作用  

Protective effect of AE3 on anoxia preconditioning via NO pathway in rat cardiomyocytes

作　　者：廖章萍[1] 刘丹[1] 王淑霞[2] 李文娟[1] 陈和平[1] 何明[1] 

机构地区：[1]南昌大学药学院药理学与分子治疗学教研室,江西南昌330006 [2]江西省人民医院,江西南昌330046

出　　处：《中国药理学通报》2012年第1期39-43,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 30760075;30960449)

摘　　要：目的从细胞水平探讨阴离子交换蛋白3(AE3)在心肌细胞缺氧预处理(APC)保护作用中的意义以及与NO通路的关系。方法以原代培养的SD新生乳鼠心肌细胞为研究对象,建立缺氧/复氧(A/R)损伤和缺氧预适应保护模型。心肌细胞随机分为4组,Control组、A/R组、APC组和NO合成酶抑制剂L-NAME组。RT-PCR和Western blot法分别测定AE3的mRNA和蛋白表达,MTT法检测细胞存活率,生化自动分析仪测定LDH、CPK活性。结果 A/R处理后,心肌细胞AE3 mRNA转录及蛋白表达较Control组略增加。APC组AE3 mRNA转录及蛋白表达不仅均较Control组转录明显上调,而且较A/R组也明显上调。但预先加入NO合成酶抑制剂L-NAME则可抑制APC处理时AE3的表达增强,并取消APC的心肌保护作用。结论 AE3可能通过NO通路参与了心肌细胞APC的保护作用。Aim To investigate the role of AE3 in anoxic preconditioning of primary cultured neonatal rat cadiomyocytes and the underlying mechanism related to NO pathway.Methods Cardiomyocytes were randomly divided into four groups as follows： control,anoxia/reoxygenation（A/R）,anoxia preconditioning（APC） and L-NAME groups.RT-PCR and Western blotting were used to measure AE3 mRNA and protein expression in A/R and APC model respectively.Cell viability was determined by MTT assay.The activity of LDH and CPK in culture medium was measured with an automatic biochemical analyzer.Results Both AE3 mRNA transcription and protein expression had upward tendency in A/R group,and had more abundance after APC,compared with A/R group and control group.However,L-NAME,an inhibitor of NO synthase inhibitor,could suppress the expression of AE3 in APC and abolished the cardioprotection of APC on cell injury and viability.Conclusion AE3 may be involved in the cardioprotection of APC via NO pathway in rat cardiomyocytes.

关 键 词：阴离子交换蛋白 缺氧/复氧 缺氧预适应 一氧化氮 信号通路 心肌细胞 

分 类 号：R-332[医药卫生] R322.11