Nicotinamide riboside alleviates hypoxia/reoxygenation injury in adult mouse cardiomyocytes via Sirt3-PGC-1α pathway

AIM To investigate the role of nicotinamide riboside (NR) in mitochondrial biogenesis in adult mouse cardiomyocytes subjected to hypoxia/reoxygenation (H/R) injury. METHODS Adult mouse cardiomyocytes were divided into four groups randomly with or without 50 μmol/L nicotinamide riboside for 48 h. After hypoxia/reoxygenation (4 h/4 h), cell apoptosis was detected by TUNEL and flow cytometry, whereas mitochondrial membrane potential was assessed by JC-1. Protein expressions of peroxisome proliferator-activated receptor co-activator 1 alpha (PGC-1α), nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (Tfam) were analyzed by Western blot. RESULTS Compared with those in the control group, H/R significantly increased the cell apoptosis index and reduced the mitochondrial membrane potential as well as the expression of PGC-1α, NRF1 and Tfam. However, NR decreased the cell apoptosis index and improved the mitochondrial membrane potential as well as the expression of PGC-1α, NRF1 and Tfam, which were reversed after knockdown of PGC-1α by siRNA. CONCLUSION Nicotinamide riboside, as a potential treatment, could improve mitochondrial biogenesis via up-regulating the expression of PGC-1α, which could eventually reduce hypoxia/reoxygenation injury in adult mouse cardiomyocytes.