Professor of the Tokyo Institute of Technology Yoshinori Osumi is successful in the Nobel Prize 2016 for the discovery of the effect of AUTOPHAGIA.
Autophagy is a natural process of regeneration that occurs at the cellular level, reducing the likelihood of some diseases and prolonging life.
- This is the process by which cells destroy and recycle their components.
- After infection with the autophagy can be destroyed bacteria and viruses
- Cells use autophagy to get rid of damaged proteins and organelles and thus fight the negative effects of aging.
- Over time, «garbage» accumulates in every cell of our body. Autophagy is a process where the lysosomes (internal organelles of the cells) of our body digest intracellular debris – including the processing of damaged cellular structures, which causes rejuvenation of the cell from the inside.
Autophagy can be caused by fasting and drugs that mimic starvation, they are called: inducers of autophagy. These include drugs attacking the target – mTOR protein, but having dangerous side effects and safe plant: SPERMIDIN and FUKOKSANTIN, which are part of the preparation NOBELbad.
Fucoxanthin has an anti-inflammatory effect, and inflammation is one of the main signs of the aging process.
Inflammation is a protective reaction of the body against various pathogenic pathogens, which is characterized by the attraction of a large number of leukocytes (neutrophils, macrophage monocytes, mast cells) to the inflammatory area to which these cells are caused by inflammatory mediators
While generating superoxide anion and nitroxyl radical, that can be a self-destructive process. Anti-inflammatory agents should reduce the inflammatory response by suppressing the production of inflammatory cytokines, such as tumor necrosis factor-a, interleukin-1β, interleukin-6, and inflammatory mediators, including synthesis of nitroxyl radical and prostaglandin E2, inducing the synthesis NO synthase and cyclooxygenase. As a result of studies, it has been shown that fucoxanthin inhibits inflammatory cytokines and mediators in lipopolysaccharide-activated macrophage cells (RAW 264.7), inhibits mast cell degranulation in vivo (Peng et al., 2011; D’Orazio et al., 2012).
The use of fucoxanthin in cosmetology. Collagen is 90% dermis skin. It is distributed throughout the dermis, making the skin elastic enough. When the collagenase enzyme is activated and the collagen is broken down, age-related phenomena such as wrinkles and sagging skin. Hyaluronic acid is widely represented in the human body, it is part of the skin, joint fluid, vitreous body and ligaments. It performs various functions, for example cell binding and protection, skin tissue formation, preservation moisture in the tissues and maintaining skin elasticity. When the quantity hyaluronic acid is reduced, the skin becomes dehydrated and loses strength, resulting in wrinkles. Hyaluronic acid in the body is broken down by hyaluronidase. Clinical studies have shown that brown algae extract, containing 8.6% fucoxanthin, slows down the activation of hyaluronidase, lowering its concentration from 30 to 1 μg / ml, thereby inhibiting the breakdown of hyaluronic acid and collagen. Similarly, inhibition of elastase activity occurs (Heo, Jeon, 2009; Urikura et al., 2011).
Dark color and dark spots on the skin are caused by melanin. Dopachinone in pigment cells (melanocytes) is produced from tyrosine in under the action of tyrosinase. Then by successive non-enzymatic reactions, including cyclization and oxidative polymerization, dopachinone is converted to 5,6-dihydrohindol and 5,6-dihydrohindol-2-carboxylic acid. Synthesized compounds are incorporated into the high molecular polymer – melanin (eumelanin). Clinical trials have shown that 8.6% fucoxanthin solution inhibits tyrosinase activity, reducing the concentration from 10 to 1 µg / ml.
In in vivo studies, guinea pigs with UV-induced pigmentation produced a product containing 1% fucoxanthin solution.
As a result, on the 12th day of the experiment, the dark spot significantly brightened, and on the 15th day it almost disappeared. So the carotenoid significantly speeds up the process of removing pigment spots (Shimoda et al., 2010; Urikura et al., 2011).
NAD + (NR)
NMN stops dysfunctions and reverberates
Adult stem cells (SC) are necessary for the maintenance and regeneration of tissues, but with aging they are susceptible to aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD (+)) and its effect on mitochondrial activity as a key switch for modulating the aging of muscle SC (MuSC) stem cells. NR also prevented the aging of MuSC in a mouse model of muscular dystrophy in mdx mice (C57BL / 10ScSn-Dmd (mdx) / J). In addition, we demonstrate that NR retards the aging of neural SC and SC melanocytes and increases the longevity of the mouse. Strategies that preserve cellular NAD (+) can reprogram dysfunctional SCs and improve longevity in mammals.