therapeutic effect of β-Nicotinamide Mononucleotide on cardiac ischemia reperfusion
Therapeutic effect of NMN on cardiac ischemia-reperfusion:
Reperfusion after cardiac ischemia is a life-threatening ischemic injury, β-Nicotinamide Mononucleotide which is accompanied by inevitable myocardial cell death and severe organ dysfunction.
Ischemic preconditioning is an endogenous defense mechanism mediated by Sirt1 that can protect myocardial viability during transient ischemia and reperfusion.
Studies have shown that NMN can protect the heart by simulating the protective effects of IPC.
After ischemia, the NAD+ content in the heart decreases.
Exogenous NMN can increase the NAD+ and NADH content in the heart and reduce the infarct size.
The data show that the reduction of the infarct size by NMN is positively correlated with the Sirt1 expression level.
In addition, β-Nicotinamide Mononucleotide the expression level of Nampt in the heart will be down-regulated under pathological conditions, β-Nicotinamide Mononucleotide such as ischemia, ischemia-reperfusion and pressure overload, β-Nicotinamide Mononucleotide which in turn affects the biosynthesis of NAD+, destroys the regulatory mechanism of Sirt1 activity, β-Nicotinamide Mononucleotide and leads to pressure overload mice Cardiomyocyte apoptosis, cardiac decompensation.
Studies have shown that in heart failure model mice, β-Nicotinamide Mononucleotide NMN treatment restores the NAD+ level in cardiomyocytes, increases the deacetylase activity of Sirt1 and the expression level of genes related to mitomycin function.
NMN improves oxidation-related degenerative diseases and physical dysfunction:
the therapeutic effect of MN on Alzheimer's disease.
With the acceleration of the aging trend of society, β-Nicotinamide Mononucleotide the incidence of Alzheimer's disease is increasing year by year.
The disease is a central nervous system disease, β-Nicotinamide Mononucleotide characterized by cognitive dysfunction and memory impairment.
Abnormality of mitochondrial structure and function is one of the pathogenesis factors of AD, β-Nicotinamide Mononucleotide and NMN promotes the energy metabolism of mitochondria and plays an important role in improving cognitive function and memory function.
*Special note - This article is for informational purposes only and cannot replace a doctor's treatment diagnosis and advice. It should not be regarded as a recommendation or proof of efficacy of the medical products involved. If it involves disease diagnosis, treatment, and rehabilitation, please be sure to go to a professional medical institution to seek professional advice.
by GSHWORLD
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