Real • 고유 한 NMN 12000mg 젊음의 분수

생산지: 캐나다

Non-medicinal ingredients: Microcrystalline cellulose, Hypromellose

*ONE OF THE PATHWAYS TO YOUTH FROM NMN

  Nicotinamide (3-Pyridinecarboxamide, Niacinamide)  

Niacinamide (aka nicotinamide) is derived from niacin. The body has the ability to convert niacin to niacinamide. However, there are some critical differences between these two vitamin B3 components. Niacinamide can also be made by our body from an amino acid known as tryptophan. High niacin doses can cause flushing, which is a condition that causes blood vessels to widen. This makes the capillaries under the skin expand to allow more blood to flow, causing the skin to become red and itchy. Niacinamide does not have the effect of skin flushing, and that is why it is preferred over niacin in the treatment of pellagra. Some niacin is converted to niacinamide, and some niacinamide is converted to a compound called NAD. Directly taking niacinamide helps “shortening” the pathway, hence speeds up the process. 

Nicotinamide, a form of vitamin B3, is a critically important part of the structures of NADH and NAD+, where the N-substituted aromatic ring in the oxidized NAD+ form undergoes reduction with hydride attack to form NADH. It is the preferred treatment for pellagra, caused by niacin deficiency. While niacin may be used, nicotinamide has the benefit of not causing skin flushing. Nicotinamide is on the World Health Organization’s List of Essential Medicines, the safest and most effective medicines needed in a health system.

  Glutamine (L-Clutamide)  

Studies have shown that Glutamine can block Oxidative stress injury induced by Reactive Oxygen Species. The mechanism by which glutamine supports cell proliferation and regulates cell cycle dynamics includes its regulation of DNA and protein biosynthesis rates. Glutamine is routinely added to the cell culture medium, and its importance for cell growth has been determined.

Oxidative stress is characterized by an imbalance between the production and elimination of cellular oxidants, which damage the basic components of cells (including proteins, lipids, and DNA), interfere with homeostasis, and lead to various adverse consequences (Schieber and Chandel, 2014; Wu and Ni, 2015). Reactive oxygen species (ROS), a marker of oxidative stress, is mainly produced in the mitochondrial electron transport chain during cell metabolism and plays important role in cell biological behaviors, such as proliferation and apoptosis (Cameron et al., 2019). Recent studies showed that ROS increases the pyroptosis of VEC that contributes to VEC dysfunction and progression (Wu et al., 2018; Zhaolin et al., 2019). Lowering oxidative stress injury induced by ROS is considered as a promising therapy to inhibit the progression of As (Burtenshaw et al., 2019).

GSH is a major endogenous cellular antioxidant that plays an important role in cellular responses to oxidative stress by neutralizing free radicals and ROS. Glutamine produces GSH and GSSG “buffers” of oxidative stress (Ballatori et al., 2009). Decreasing glutaminase and consequently inhibiting glutamine production can down-regulate this important antioxidant pathway, leading to high ROS levels and toxic effects on cells (Abu et al., 2017). Glutamine starvation has been reported to deplete endogenous levels of the antioxidant GSH, promote oxidative stress in HuH-7 cells, and induce apoptosis (Yang et al., 1998). ECS is highly susceptible to ROS-induced damage because of glutamine consumption (Huang et al., 2017). In addition, glutamine-starved ECs are more sensitive to ROS-induced cell death (Huang et al., 2017). Similarly, glutamine-depleted ECs show a tendency to decrease the overall level of GSH (Huang et al., 2017). Thus, glutamine supplementation reduces mitochondrial ROS formation and apoptosis induced by high glucose and hypoxia re-oxygenation by decreasing oxidative stress and inactivating intrinsic apoptosis pathways. This process is mainly dependent on enhanced GSH synthesis (Li et al., 2015).

  Pterostilbene (4′-Hydroxy-3, 5-demethoxystilbene)  

Animal studies have found that Pterostilbene, as a strong antioxidant, is absorbed by human blood four times higher than resveratrol. Its utilization rate of biological activity in the human body is 80%, while that of resveratrol is only 20%. According to research, Pterostilbene can protect cell DNA and is the protective cap of the telomere at the end of the DNA chain. As we age, telomeres will naturally start to break down, and Pterostilbene can enhance the enzymes that protect telomeres. Taking Pterostilbene can help improve the body’s natural anti-aging ability and promote overall wellness. It also promotes the body to release adiponectin, a hormone that helps regulate blood sugar and fatty acid metabolism.

  NADH (Nicotinamide adenine dinucleotide (NAD) + Hydrogen (H))  

NADH is made in your body from niacin, a type of B vitamin. At various chemical reactions, the NAD+ picks up an electron from glucose, at which point it becomes NADH. Then NADH, along with another molecule flavin adenine dinucleotide (FADH2) will ultimately transport the electrons to the mitochondria, where the cell can harvest energy stored in the electrons. The amount of NADH is directly related to the amount of ATP produced. The more NADH each cell has, the more energy it produces. Organs that require more energy have more (or require) NADH.

Physiological Functions of NADH: 

• Improves energy levels: A large number of studies have confirmed that extracellular NADH can promote the rise of the level of ATP in the cell. It has been shown that NADH can penetrate the cell membrane and raise the level of energy in cell. From the macro added exogenous, NADH helps restore physical strength, enhance appetite, and raise the level of brain energy. It also helps to improve mental state and sleep quality. NADH has been applied to improve chronic fatigue syndrome, improve sports endurance, jet lag, and other fields in foreign countries.
• Protects cells: NADH is a naturally occurring strong antioxidant. It can react with free radicals and inhibit lipid peroxidation, protecting the mitochondrial membrane, and mitochondrial function. A study found that NADH can reduce ischemia toxins by radiation medicine, violent sport oxidative stress caused by various factors, such as cells, thus protecting myocardial vascular endothelial cells of liver cells fibroblasts neurons. Therefore, the injection or oral intake of NADH in the clinic is applied to improve the disease of heart head blood-vessel auxiliary cancer radiation and chemotherapy, and other fields. Topical NADH has been shown to be effective in the treatment of rosacea and contact dermatitis.
• Promotes the neurotransmitter produced: Studies have shown that NADH is significant to promote the production of the neurotransmitter dopamine, which proved critical to the central nervous system functions such as movement, pleasure, attention, mood, and motivation. Dopamine is a messenger molecule in the brain that allows certain nerve cells to communicate with one another. It also mediates the release of growth hormone and determines muscle movement. Without enough dopamine, muscle stiffness, for example, will become part of the etiology of Parkinson’s disease which is caused by brain dopamine synthesis disorder. Preliminary clinical trial data suggests that NADH contributes to the improvement of the symptoms of Parkinson’s disease. NASH also promotes the biosynthesis of norepinephrine and serotonin, showing promising application potential in alleviating depression and Alzheimer’s disease

In metabolism, NAD facilitates redox reactions, carrying electrons from one reaction to another. This means that NAD is found in two-forms in the cell; NAD+ is an oxidizing agent that takes electrons from other molecules in order to become its reduced form, NADH. NADH can then become a reducing agent that donates the electrons it carries. The transfer of electrons is one of the main functions of NAD, though it also performs other cellular processes, including acting as a substrate for enzymes that add or remove chemical groups from proteins in post-translational modifications.

NAD + and NADH is the cell of a pair of REDOX, NADH is a reductive form of coenzyme NAD 1, NAD + is the oxide forms in REDOX reaction, NADH as hydrogen and electron donor, NAD + as a hydrogen and electron acceptor, involved in alcohol metabolism and other physiological respiration photosynthesis process them as in many REDOX reactions of coenzyme body to participate in the activities of life, and into each other. In the absence of oxygen, glucose metabolism produces very little ATP. Under aerobic conditions, NADH or FADH2 produced by glycolysis and the tricarboxylic acid cycle can produce a large amount of ATP by the oxidative phosphoric acid reaction.