OBJECTIVE: To determine the protective effect of nicotinamide on chronic hypoxic myocardial cells and its underlying mechanism.
MATERIALS AND METHODS: The H9C2 cell lines were taken as objects of study, and were divided into blank group, hypoxia group and nicotinamide treatment group. The cell viability, apoptosis level, autophagy level and mammalian target of rapamycin (mTOR) pathway activity in each group were detected via Cell Counting Kit-8 (CCK8) assay, Hoechst staining, immunofluorescence staining, Polymerase Chain Reaction (PCR) and Western blotting, respectively.
RESULTS: Nicotinamide could protect the viability of normoxic and chronic hypoxic myocardial cells. Besides, it could also inhibit the expression of caspase3 messenger ribonucleic acid (mRNA) in chronic hypoxic myocardial cells, and reduce the expression of apoptosis-related proteins. Furthermore, it could induce the mRNA expression of autophagy-associated gene 5 (ATG5) and increase the expression of autophagy-related proteins. Further study on the mechanism of nicotinamide showed that nicotinamide could inhibit the activity of the mTOR pathway, thus regulating the autophagy.
CONCLUSIONS: Nicotinamide induces the autophagy of chronic hypoxic myocardial cells by regulating the mTOR pathway, thereby protecting cells from apoptosis.
To cite this article
W. Li, L. Zhu, Z.-B. Ruan, M.-X. Wang, Y. Ren, W. Lu
Nicotinamide protects chronic hypoxic myocardial cells through regulating mTOR pathway and inducing autophagy
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 12