中国药理学通报2018，Vol.34Issue(7)：964-969,6.DOI:10.3969/j.issn.1001-1978.2018.07.015
基于VDAC1/mPTP调节机制探讨葛根素抗心肌细胞缺氧/复氧损伤的保护作用
Protective effect of puerarin against anoxia reoxygenation injury in cardiomyocytes based on VDAC1/mPTP regulation mechanism
摘要
Abstract
Aim To study the effect of puerarin( Pue) against myocardial ischemia/reperfusion injury and in-volved mitochondrial mechanism. Methods Anoxia/reoxygenation( A/R) injury model was established in H9c2 cell. Recombinant plasmid pFLAG-VDAC1 was constructed. Cells were randomly divided into 4 groups, normal control group ( Control) , A/R group, puerarin group ( Pue + A/R ) , and pFLAG-VDAC1-Pue group. Real-time PCR was used to investigate the expression of VDAC1 at mRNA level, and the expres-sion of protein level was detected by Western blot. LDH and CK activities were measured by automatic bi-ochemical analyzer. Mitochondrial membrane potential ( Δψm) and cell apoptosis were observed by flow cy-tometry method. Mitochondrial swelling test was used to detect the opening of mitochondria permeability tran- sition pore ( mPTP) . Results Compared with control group, the expression of VDAC1 and mRNA was up-regulated in A/R group, LDH and CK activity were el-evated, and then mPTP opened, Δψm collapsed, cell apoptosis was significantly increased. Puerarin pre-treatment can lower the expression of VDAC1, main-tain Δψm, prevent the opening of mPTP, and reduce apoptosis. However, the protective effect of Puerarin could be cancelled by transfection of pFLAG-VDAC1. Conclusions The cardioprotection of Puerarin against A/R injury is closely related to down-regulation of VDAC1 and prevention of mPTP opening.关键词
葛根素/缺氧/复氧损伤/细胞凋亡/电压依赖性阴离子通道1/线粒体通透性转换孔道/心肌细胞Key words
puerarin/anoxia/reoxygenation injury/apoptosis/VDAC1/mitochondrial permeability transi-tion pore/cardiomyocytes分类
医药卫生引用本文复制引用
马文,徐勇民,孟艳,贺敏,杨小梅,何明,廖章萍..基于VDAC1/mPTP调节机制探讨葛根素抗心肌细胞缺氧/复氧损伤的保护作用[J].中国药理学通报,2018,34(7):964-969,6.基金项目
国家自然科学基金资助项目(No 81460495,81660601) （No 81460495,81660601）
南昌大学研究生创新基金资助项目(No cx2016381) （No cx2016381）
