Sirt1 improves heart failure through modulating the NF-κB p65/microRNA-155/BNDF signaling cascade
Bin Lin, Hui Zhao, Li Li, Zhenzhen Zhang, Nan Jiang, Xiaowei Yang, Tao Zhang, Bowen Lian, Yaokai Liu, Chi Zhang, Jiaxiang Wang, Feng Wang, Deguang Feng, Jing Xu
Abstract
, 30 min) in cardiomyocytes harvested from suckling rats. HF rats presented with downregulated expressions of Sirt1, brain-derived neurotrophic factor (BDNF) and exhibited upregulated expressions of NF-κB p65 and miR-155. Repressed Sirt1 expression increased acetylation of NF-κB p65, resulting in the elevation of NF-κB p65 expression. NF-κB p65 silencing improved heart functions, decreased ventricular mass and reduced apoptosis in cardiomyocytes. MiR-155 inhibition upregulated its target gene BDNF, thereby reducing cardiomyocyte apoptosis. Sirt1 overexpression upregulated BDNF, improved heart function, and reduced apoptosis in cardiomyocytes. In conclusion, Sirt1 alleviates HF in rats through the NF-κB p65/miR-155/BDNF signaling cascade.