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Therapeutic Effect of Nicotinamide Mononucleotide on Cardiac Ischemia-reperfusion Therapeutic Effect of Nicotinamide Mononucleotide on Cardiac Ischemia-reperfusion

NMN (nicotinamide mononucleotide) is a product of the Nicotinamide phosphate ribose transferase (Nampt) reaction and is one of the key precursors of NAD+. The CAS number of the NMN is 1094-61-7. In mammals, NMN is produced by Nicotinamide (Nam) catalyzed by Nampt. Subsequently, NMN produces NAD+ under the catalysis of nicotinamide mononucleotideadenosine transferase (Nmnat).
Reperfusion after cardiac ischemia is a life-threatening ischemic injury. This process is accompanied by inevitable myocardial cell death and severe organ dysfunction. Ischemic preconditioning (IPC) is a mechanism that protects myocardium during transient ischemia-reperfusion by activating Sirt1-mediated endogenous defense mechanisms. Studies have shown that NMN protects the heart by mimicking the protective effects of IPC. The content of NAD+ in the heart after ischemia decreased. Exogenous NMN increased the content of NAD+ and NADH in the heart and decreased the infarct size. The data showed that the size of infarct size decreased by NMN was positively correlated with the expression level of Sirt1. In addition, the expression level of Nampt in the heart is down-regulated under pathological conditions such as ischemia, ischemia-reperfusion, and pressure overload. Furthermore, it affects the biosynthesis of NAD+, destroys the regulation mechanism of Sirt1 activity, and leads to myocardial apoptosis and cardiac decompensation in pressure overload mice. In mouse experiments, NMN treatment restored NAD+ levels in cardiomyocytes and increased the deacetylase activity of Sirt1 and gene expression levels associated with mitomycin function in model mice with heart failure. It can be seen that supplementing NMN and increasing the level of NAD+ in the body is particularly necessary.
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