Anti-free radical damage
The theory of free radicals has been recognized as the mechanism of skin aging. Oxygen participates in the respiratory chain process of organisms, but it is also the source of reactive oxygen species (ROS). With the growth of age and the decline of antioxidant enzyme activity, the generation of oxygen free radicals increases and the scavenging effect weakens, resulting in excessive accumulation of ROS in the skin, causing damage to cell membranes, proteins and nucleic acids. ROS can activate the mitogen-activated protein kinase (MAPK) pathway in the body and eventually destroy the skin structure. The MAPK pathway includes four pathways: extracellular signal-regulated protein kinase (ERK ), c-Jun N-terminal kinase (c-Jun N-terminal kinase, JNK), extracellular signal-regulated protein kinase 5 (extracellular signal-regulated protein kinase5, ERK5), p38 mitogen-activated protein kinase (p38 mitogen-activated protein kinase, p38MAPK). Among them, JNK can activate activated protein-1 (AP-1), which in turn stimulates the production of matrix metalloproteinases (MMPs). MMPs are a group of zinc-dependent endopeptidases that play complex roles in many physiological and pathological processes including skin aging. MMP-1 can degrade the intact collagen and elastin in the dermis, and the activation of the MAPK pathway can inhibit the production of procollagen DNA, which eventually leads to the destruction of the dermal structure and the formation of skin aging.
Inhibit telomere shortening
Telomeres are repetitive DNA sequences at the ends of chromosomes. The length of telomeres is directly proportional to the number of cell divisions. Telomere length is the longest at birth and gradually shortens with age. Normal human cells have a certain number of divisions, so the shortening of telomeres is considered to be related to the aging of the body. Telomerase lengthens telomeres. Shao et al. found that growth of fibroblasts in a medium containing 20 mmol/L carnosine can slow down the shortening of telomeres and prolong the lifespan of cells. Therefore, it is believed that reducing telomere shortening and telomere DNA damage is one of the mechanisms by which carnosine can prolong life.
Anti-glycosylation
Protein glycosylation is one of the important processes of protein post-translational modification. The aldehyde-containing sugar and the amino residues of the protein are connected under the condition of no enzyme, and the Schiff base (Schiff base) is first formed, and then after a period of rearrangement, a relatively stable early glycosylation product, that is, a ketone amino compound is formed. (amadori product), after dehydration and rearrangement, the amadori product forms a highly active carbonyl compound such as malondialdehyde (malondialdehyde, MG), etc., and then reacts with the free amino group of the protein to form a more stable form through cyclization, oxidation and dehydration advanced glycosylation end products (AGEs). This process is called the Maillard reaction. As we age, AGEs also accumulate, causing damage to tissues and organs. The dermis is mainly composed of collagen fibers, elastic fibers and extracellular matrix produced by fibroblasts. Elastin and collagen participate in non-enzymatic glycosylation reactions to generate AGEs, forming cross-linked products of collagen and elastin. Oxidized collagen can be degraded by collagenase at the beginning. As the cross-linking of collagen gradually increases, the dissolution of collagen Decreased elasticity and accumulation of insoluble collagen lead to a decrease in tissue permeability, resulting in barriers to the exchange of nutrients and metabolites between cells, and ultimately lead to a decrease in skin elasticity and wrinkles. l Carnosine Tablet can react with active substances in the body to protect proteins from glycosylation, while carnosine can interact with glycosylated protein products to prevent further cross-linking of glycosylated proteins.
Rejuvenate aging cells
As early as 1994, McFarland and Holliday observed the effect of l Carnosine Tablet on the growth, shape and lifespan of fibroblasts in experiments. They found that high concentrations of carnosine (20-50 mmol/L) can delay aging and rejuvenate already aged fibroblasts. In the presence of carnosine, fibroblasts that had divided close to the Hayflick demarcation could assume an unsenescent form, and when these cells were transferred to cultures without carnosine, they quickly reverted to senescence form
Anti-tumor effect
The occurrence of tumors is inseparable from aging. With age, the incidence of tumors also increases significantly, which may be related to the gradual decline of DNA damage repair function with age. At the same time, oncogenes can induce cell senescence. Scientists have found that even in the presence of oxygen, tumor cells still preferentially use glucose for aerobic glycolysis to produce lactic acid to produce ATP, a phenomenon known as the Warburg effect. Therefore, it can be inferred that inhibiting the glycolytic activity of tumor cells can inhibit the proliferation of tumors. Ding et al found by measuring the survival rate of human liver cancer cells that l Carnosine Tablet can significantly inhibit the growth of tumor cells, and this phenomenon is concentration-dependent. And it is inferred that carnosine may be used to inhibit the proliferation of human tumor cells in the future to achieve the purpose of anti-tumor.
Regulating autophagy and apoptosis
Autophagy and apoptosis are closely related to aging and aging-related diseases. Autophagy is the self-digestion process of cells through lysosomes to intracellular metabolites, such as abnormally modified proteins, protein aggregates and damaged organelles. Therefore, autophagy can control the quality of intracellular proteins and organelles to maintain the stability of the intracellular environment. The reduction of autophagy can be observed in many aging models, and up-regulation of autophagy through pharmacological and genetic methods can alleviate the occurrence of age-related diseases, but on the other hand, excessive autophagy can accelerate aging.
Others
l Carnosine Tablet is a rapamycin analogue. The activation of the mammalian target of rapamycin (mTOR) pathway is the driving force leading to cell aging. Carnosine can inhibit the mTOR signaling pathway. Enhanced cell cycle arrest to suppress UVA-induced senescent phenotype of dermal fibroblasts. In summary, the anti-aging mechanism of carnosine is mainly anti-oxidation, inhibition of telomere shortening, inhibition of mitochondrial damage, anti-glycosylation, and anti-tumor effects. It can not only inhibit cell aging, but also delay the progression of some diseases related to aging. Development occurs. Although there have been some studies, there are not many studies on carnosine in anti-aging skin.
