Recombinant adeno-associated virus serotype 9 with p65 ribozyme protects H9c2 cells from oxidative stress through inhibiting NF-κB signaling pathway  

作　　者：Zhan SUN Yi-Tong MA Bang-Dang CHEN Fen LIU 

机构地区：[1]Xinjiang Key Laboratory of Cardiovascular Disease Research, Urumqi 830054, Xinjiang Uygur Autonomous Region, China [2]Laboratory of Functional Experiment, Preclinical Medicine, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China [3]Department of Cardiology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China

出　　处：《Journal of Geriatric Cardiology》2014年第4期311-315,共5页老年心脏病学杂志（英文版）

基　　金：the National Natural Sci-ence Foundation of China，China Post-doctoral Science Foundation

摘　　要：Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB （NF-κB）. The NF-κB transcription factor family includes several subunits （p50, p52, p65, c-Rel, and Rel B） that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Mechods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme （AAV9-R65-CMV-eGFP） was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the under-lying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65-CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease.

关 键 词：CARDIOMYOCYTES ADENOVIRUS R65 ribozyme Apoptosis NF-κB pathway 

分 类 号：Q782[生物学—分子生物学] Q463