中国药理学通报2013，Vol.29Issue(1)：48-52,5.DOI:10.3969/j.issn.1001-1978.2013.01.011
Bcl-2/Bad/mPTP通路介导14-3-3γ对抗脂多糖所致心肌损伤
Bcl-2/Bad/mPTP pathway mediates 14-3-3γ protecting against LPS- induced myocardial injury
摘要
Abstract
Aim To explore the role of Bcl-2／Bad／mPTP pathway in 14-3-3γprotecting against LPS-in-duced cardiomyocyte injury.Methods pFLAG-14-3-3γrecombinant lasmid was constructed and transfect-ed into primary neonatal SD rat cardiomyocytes.After treatment of LPS injury,the activity of LDH was ana-lyzed in supernatant;cell viability was detected by MTT colorimetric assay;cell apoptosis was determina-ted by flow cytometry;opening of mitochondrial perme-ability transition pore(mPTP)was detected by swelling of isolated cardiac mitochondria;the level of 14-3-3γ,Bad,phospho-Bad protein in cell and the level of Bcl-2 protein in mitochondria were analyzed bv Western blot.Results LPS damage made LDH activity increase,cell viability decrease,cell apoptosis increase,and mPTP opening aggravate.After the transfection with pFLAG-14-3-3γ,LDH activity and cell apoptosis were decreased,cell viability was increased,mPTP opening was inhibited,and level of phospho-Bad was raised,while level of Bcl-2 in mitochondria was also increased. Conclusions pFLAG-14-3-3γcan protect against LPS-induced cardiomyocyte damage,and the mecha-nism is related to phosphorylating Bad,releasing Bcl-2 to mitochondria,and inhibiting mPTP opening.关键词
Bcl-2/Bad/线粒体/mPTP/质粒转染/脂多糖/心肌损伤Key words
Bcl-2/Bad/mitochondria/mPTP/plas- mid transfection/lipopolysaccharide/myocardial injury分类
医药卫生引用本文复制引用
刘丹,彭易安,刘卓琦,汤蕾,尹东,何明..Bcl-2/Bad/mPTP通路介导14-3-3γ对抗脂多糖所致心肌损伤[J].中国药理学通报,2013,29(1):48-52,5.基金项目
国家重点基础研究发展计划(973计划)资助项目(No 2009CB 526405) （973计划）
国家自然科学基金资助项目(No 81160402,81072632) （No 81160402,81072632）
