Oct 05, 2024 / Author: China Glutathione suppliers & NMN manufacturers
Cardiovascular and cerebrovascular diseases pose a serious threat to people's physical health. Today, we have summarized multiple research results of NMN on cardiovascular and cerebrovascular diseases.
NMN can activate Sirtuins in our body. It is also known as silencing regulatory protein, which is a NAD+- dependent class III histone deacetylase in mammals. By regulating the acetylation levels of various proteins in cells, it plays a key regulatory role in the growth, development, aging, and various diseases of the body.
In recent years, research has found that Sirtuins are closely related to vascular remodeling diseases through multiple mechanisms.
After oral administration, NMN can be quickly absorbed by the human body and penetrate the cell membrane, thereby synthesizing NAD+in cells, increasing the level of NAD+in the human body, and reversing the process of vascular aging, acting on the prevention and improvement of cardiovascular and cerebrovascular diseases.
Cerebral infarction is the most common type of cerebrovascular disease, accounting for about 70% of all acute cardiovascular and cerebrovascular diseases, and is more common in middle-aged and elderly patients. The ratio of female to male patients is 1:1.
Researchers have found that NMN can prevent cerebral infarction. In 2019, researchers from the Department of Geriatrics at the Health Science Center in the United States discovered that NMN can enhance the relaxation of endothelial cells and promote blood circulation.
After entering the cell, NMN can effectively increase the content of NAD+, which in turn enhances the expression of SIRTUINS, thereby reducing the attack of free radicals on mitochondria in the cell, maintaining mitochondrial function, and enabling mitochondria to produce nitric oxide.
This is a very important cell relaxant, and the release of nitric oxide greatly enhances the degree of vasodilation, thereby promoting the circulation of cardiovascular and cerebrovascular systems, and effectively improving cognitive function.
This theory not only provides theoretical support for NMN to effectively enhance endothelial cell relaxation and improve brain tissue blood supply, but also provides a new research direction for preventing cerebral infarction and improving brain cognitive function.
Cerebral hemorrhage (ICH) is a primary brain injury caused by mechanical damage, resulting in hematoma.
It may sometimes develop into secondary injury, mainly due to subsequent pathophysiological changes, including blood-brain barrier (BBB) disruption, hemoglobin induced iron overload, neuronal cell death, neuroinflammation, and oxidative stress.
It often occurs in patients over 50 years old with a history of hypertension, and has a high mortality and disability rate, posing a serious threat to people's health.
Research has found that NMN can activate the NAD+defense system, protect brain nerves, and promote nerve regeneration of blood vessels. It has a good repairing effect on nerve damage caused by cerebral hemorrhage and its transformation, and is a potential anti stroke treatment drug.
NMN has a protective effect on ischemic brain injury.
In addition, further research by the scientific team has shown that NMN enhances the expression of cell protective proteins, inhibits neuroinflammation and oxidative stress, and reduces damage after intracerebral hemorrhage.
Healthy arteries have elasticity, but over time, the arterial wall will harden, a condition commonly known as arteriosclerosis.
In May 2019, Kiss Tamas and other scientists from the Department of Geriatrics of the University of Oklahoma Health Science Center showed that NMN can reverse a level called MIRNA in blood vessels, make epigenetic young and resist atherosclerosis through experimental research on mouse models. In short, NMN can prevent atherosclerosis and prevent vascular aging.
Vascular aging is one of the direct causes of aging in the body, and how to keep blood vessels young has become a research focus in the field of aging inhibition.
A study co authored by Xin Hongbo from Nanchang University and Xue Jianxin and Gan Lu from West China Hospital of Sichuan University shows that:
The decrease in intracellular NAD+(nicotinamide adenine dinucleotide) levels caused by CD38 (one of the NAD+metabolic pathways) is an important cause of age-related cardiovascular and cerebrovascular diseases.
Supplementing with NMN (β - Nicotinamide Mononucleotide) or inhibiting CD38 can increase NAD+levels, delay the aging of mouse vascular smooth muscle cells, and induce pathological structural changes.
Research has found that CD38 not only decomposes NAD+, but also consumes precursor substances such as NMN necessary for synthesizing NAD+. Compared with normal mice, the NAD+level in aortic cells of CD38 gene deficient mice increased by nearly 50%.
To explore whether NAD+supplements can salvage the aging of vascular smooth muscle cells, researchers orally administered NMN (300mg/kg) to normal mice.
The results showed that the NAD+level in the mice increased, and the symptoms of hypertension induced by angiotensin II were improved. The thickness of the vascular media, the ratio of media to lumen, and collagen deposition were reduced by 26%, 27%, and 30%, respectively.
In April 2022, a research team from Fudan University Children's Hospital and School of Life Sciences published their findings in JACC (Journal of the American College of Cardiology)
NMN can effectively inhibit cardiac dysfunction caused by Echs1 deficiency. Of course, this is not the first time NMN has unlocked the function of protecting the heart.
Echs1 (short chain acetyl CoA hydratase 1) is a key enzyme involved in the oxidation of fatty acids (FA) and branched chain amino acids (BCAA), and is closely related to the occurrence of cardiomyopathy.
And researchers have found that ECHS1 can regulate histone acetylation, so the etiology of ECHS1 related cardiomyopathy may be due to the lack of ECHS1 leading to dysregulation of histone acetylation in cardiac fibroblasts.
NMN can mediate histone acetylation and target the development of ECHS1 deficient cardiomyopathy, making NMN supplementation a potential preventive measure for cardiomyopathy.
From 2011 to 2014, scientists discovered through research that NMN can reduce the degree of arteriosclerosis in mice and improve vascular wall elasticity.
The overall drug literacy of cardiovascular disease patients still needs to be improved, and the level of drug literacy is influenced by multiple factors that can affect patients' medication compliance and lead to adverse health outcomes.
After feeding elderly mice with NMN, scientists measured arterial stiffness and elasticity through active pulse wave velocity (aPWV). The results showed that the vascular wall stiffness of older mice fed with NMN was lower than that of older mice not fed with NMN, and close to that of young mice.
And the elastic modulus is also smaller. The smaller the elastic modulus, the better the elasticity. The larger the elastic modulus, the greater the stiffness of the blood vessel wall, and the harder the blood vessel wall.
When a person's blood vessel wall is young, it is like a soft candy with good elasticity and can be easily retracted. As age increases, the collagen and elastin on the blood vessel wall gradually decrease, but the loading protein gradually increases.
Elastic glial cells continue to lose, but hard substances continue to increase, causing the blood vessel wall to gradually become hard and brittle, without elasticity, and easily break.
Scientists have discovered that feeding aging mice with NMN results in a lower protein load compared to regular aging mice, while the amount of elastin is higher. This proves that NMN can increase the elastin content of aging blood vessel walls, thereby enhancing vascular elasticity.
In 2020, a study conducted by the University of Washington in the United States tested the effects of two different mitochondrial targeted drugs, SS-31 and NMN, and found that SS-31 partially reversed age-related diastolic dysfunction, while NMN completely reversed age-related cardiac systolic dysfunction.
The synergistic effect of the two can better restore vitality to the aging heart.
Coronary atherosclerosis, abnormal heart metabolism, myocardial ischemia and other factors may lead to cardiac fibrosis, which will lead to abnormal cardiac stiffness, and ultimately lead to heart failure.
Supplementing NMN also has a good protective effect on blood vessels, which can reduce cardiovascular disease, improve heart disease and vascular dysfunction. Taking NMN can restore the activity of Sirt1 in blood vessels, delay the decline of endothelial cell number and function, and improve endothelial dysfunction and large elastic arteriosclerosis caused by aging.
Numerous studies have confirmed that supplementing with NMN has a very good protective effect on heart disease and vascular sensitivity. NMN comprehensively and effectively revitalizes the cardiovascular system and plays a significant role in the prevention and treatment of cardiovascular and cerebrovascular diseases.
Supplier Introduction: China glutathione supplier and NMN manufacturer GSHworld, the company mainly develops biotechnology and industrialization. As a global pioneer in enzymatic catalytic ATP regeneration technology, our company advocates green production and is committed to providing customers with better and more environmentally friendly products and services. Glutathione Manufacturer,NMN Factory,Citicoline Sodium supplier,China NMN manufacturers
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