Nicotinamide mononucleotide improves oxidative related degenerative diseases and physical dysfunction
Therapeutic effect of nicotinamide mononucleotide on Alzheimer's disease
With the acceleration of social aging trend, the incidence rate of Alzheimer's disease (AD) increases year by year. The disease is a central nervous system disease, which is characterized by cognitive dysfunction and memory impairment. The abnormality of mitochondrial structure and function is one of the pathogenic factors of AD, and nicotinamide mononucleotide promotes mitochondrial energy metabolism, which plays an important role in improving cognitive function and memory function. It was found that when the nicotinamide mononucleotide level in the body was increased, the availability of NAD+increased, the mitochondrial oxygen consumption rate (OCR) was increased, the mitochondrial fusion was promoted, the fission trend was reduced, and the mitochondria produced longer mitochondria in the hippocampus subregion, thus improving the respiratory function of mitochondria. β- Amyloid oligomer β protein，A β) It is considered to be the main nerve agent causing AD. It is found that nicotinamide mononucleotide can improve energy metabolism, inhibit oxidative stress, and improve β The cognitive and memory functions of Alzheimer's disease rats induced by 1-42 oligomers restored the levels of NAD+and ATP, and reduced the accumulation of ROS (reactive oxygen species) in the hippocampal slices of AD mice. The study found that nicotinamide mononucleotide improved the behavioral cognitive impairment of AD mice and inhibited the β- Amyloid protein production can reduce the load of amyloid plaque in nervous system, synaptic damage and inflammatory reaction. The above experiments show that nicotinamide mononucleotide can be used as a potential drug to treat AD.
Therapeutic effect of nicotinamide mononucleotides on Parkinson's disease:
Parkinson's disease (PD) is a degenerative disease of the central nervous system that occurs in the elderly, with the main clinical manifestations of motor symptoms such as motor retardation, static tremor, rigidity, abnormal gait and posture, and non motor symptoms such as hypoesthesia, anxiety and depression, constipation. The pathogenesis of the disease is relatively complex and still unknown, so there is almost no effective treatment. Studies have shown that nicotinamide mononucleotide can improve the survival rate of nerve cells, reduce cell apoptosis, restore the levels of NAD+and ATP, inhibit cell apoptosis, resist energy damage, and improve the energy metabolism disorder induced by mitochondrial inhibitors. Compared with Alzheimer's disease, there are few studies on the effect of nicotinamide mononucleotide on Parkinson's disease, and more in vivo experimental data are needed to prove its effectiveness.
The therapeutic effect of nicotinamide mononucleotides on vascular disorders
Another serious health threatening disease related to aging is cardiovascular diseases (CVD), which is characterized by high incidence rate, high disability rate, and wide harm to people. This kind of disease is mainly due to the imbalance between the oxidation system and the antioxidant system after the aging of the body, and the accumulation of superoxide in the blood vessels, resulting in oxidative damage to the body. It is found that NMN supplementation can reduce vascular oxidative stress, improve aortic sclerosis and vascular dysfunction; Nicotinamide mononucleotide supplementation can reduce the accumulation of collagen in the whole blood vessel, increase the accumulation of arterial elastin, reduce arteriosclerosis, and delay the aging of arteries with age. Nicotinamide mononucleotide mainly increases the bioavailability of NAD+in the vascular system, restores the activity of Sirt1 in arteries, and improves endothelial dysfunction and large elastic arteriosclerosis caused by aging. Nicotinamide mononucleotides can also maintain the antioxidant system of glutathione and thioredoxin by enhancing the metabolic flux of the tricarboxylic acid cycle and the electron transfer chain, reducing the accumulation of reactive oxygen species in cells, and increasing the level of NADPH (reduced nicotinamide adenine dinucleotide phosphate). In addition, nicotinamide mononucleotide can also improve the lipid distribution in plasma and maintain blood glucose level, thereby improving vascular function.
The therapeutic effect of nicotinamide mononucleotide on acute renal injury
The incidence rate and mortality of acute renal injury (AKI) are increasing year by year, which has attracted more and more attention. The research shows that the levels of Sirt1 and NAD+decrease with age; The decrease of NAD+and Sirt1 in the kidney of the aged organism will lead to the increase of AKI susceptibility; Nicotinamide mononucleotide supplementation can protect mice from AKI induced by cisplatin (which can be used to inhibit DNA replication); The mechanism of NAD+/Sirt1 protecting kidney involves epigenetic regulation of JNK pathway; In vitro, Sirt1 attenuates stress response by regulating JNK signaling pathway. Endogenous NAD+is considered as a potential therapeutic target of AKI in the elderly, and it is a good therapeutic strategy to supplement the intermediate nicotinamide mononucleotide of NAD+.
Anti aging effect of nicotinamide mononucleotide
The study found that nicotinamide mononucleotide can significantly improve the age-related physiological decline of mice, such as inhibiting age-related weight gain, enhancing energy metabolism, improving insulin sensitivity and lipid distribution in plasma, and improving eye function; Nicotinamide mononucleotides prevent age-related gene expression changes in a tissue specific manner, and enhance the oxidative metabolism of mitochondria in skeletal muscle, at least partially mediating its anti-aging effect.
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