Scientists have discovered two drugs that restore the key collagen content of the skin April 08, 2019 Source: Singularity Network I don't know when, the sea cucumber, pig's trotters and other collagen-rich foods are labeled as beauty and beauty. Even the jelly-like food consisting of peach gum has to look at the hot spots of collagen, claiming that it also has a cosmetic function. As for the almost pure collagen gelatin, it is even more expensive. Although the beauty foods bearing the collagen flag are basically collected by the IQ tax, the beauty of collagen is true. It's just that this supplement is not to say that the protein that is eaten can't be absorbed as it is, but this absorption efficiency can be seen by looking at the repeated oral insulin preparations [1]. Recently, Nan liu and Emi K. Nishimura of Tokyo Medical and Dental University found that under the influence of various damage factors, a collagen called COL17A1 in the skin is reduced, leading to skin aging. And they also found a way to effectively "supplement" COL17A1 collagen and make the skin more "young." Related research was published in Nature [2]. As the first line of defense for our body, the skin is exposed to the sun and rain of the outside world, and these will cause damage to the skin and accelerate the aging of the skin [3]. Intrinsic factors such as poor diet and diabetes also accelerate skin aging [4]. The thickness of the aging skin is thinner, loses its elasticity, appears pigmentation, and the healing ability after injury is not as good as before. In particular, the reduction of collagen, which constitutes hemidesmosome, such as COL17A1, makes aging skin particularly vulnerable [5]. Our skin consists of the epidermis of the outermost layer of epithelial tissue and the dermis and subcutaneous tissue of connective tissue inside the epidermis. There is a thin base film between the epidermis and the dermis. The basal cells in the deepest part of the epidermis are firmly attached to the basement membrane by the semi-bridge particles [6]. The bullous epidermolysis of bloody bubbles at the touch of a cell, the mutation of collagen such as COL17A1 makes the hemidesmosome lose its function [7]. In addition to attaching the epidermis to the basement membrane, the basal cells at the deepest part of the epidermis are also the source of other cells in the epidermis. The stem cells and progenitor cells of the epidermis are among them, which is especially important for epidermal renewal and damage repair. To further investigate skin aging, the researchers tested on the tail skin of mice. Like human skin, the skin on the tail of mice is well stratified. When aging, the number of epidermal cell layers is reduced, basal cells are flattened, and cell proliferation activity is weakened. In addition, in the tail skin of aged mice, the number of hemides that connect the epidermis and the basement membrane is greatly reduced. The analysis of various semi-bridged components showed that, like human skin, the content of collagen COL17A1 in the tail skin of mice decreased significantly with age. Next, the researchers tested the effects of various physical and chemical factors that accelerate skin aging, such as ultraviolet light, ionizing radiation, and hydrogen peroxide, on the level of COL17A1 in the skin. These factors, which can cause genomic damage, can reduce the level of COL17A1 in the skin. . Moreover, COL17A1-deficient mouse skin is more susceptible to aging, has reduced wound healing ability, and is more prone to pigmentation when exposed to ultraviolet light. The overexpression of COL17A1 also makes the wound healing ability of the skin of the mouse stronger, and it is less prone to pigmentation under ultraviolet irradiation. The level of COL17A1 is related to genetic damage, so will it affect cell proliferation? The researchers asked mouse epidermal cells to randomly express red, yellow, green or cyan fluorescent proteins. When they were young, these different colored fluorescent cells were evenly and randomly distributed on the skin. But when old, there was a large monochromatic area in the skin of these mice. More importantly, the size of these monochromatic areas in old mice is positively correlated with the expression level of COL17A1! Highly expressed cells of COL17A1 have a competitive advantage! Further studies have found that COL17A1-positive cells tend to undergo horizontal division (also known as symmetric division), creating two new cells that are also attached to the basement membrane, occupying more space. COL17A1-negative cells prefer vertical division (also known as asymmetric division), in which one daughter cell enters the superficial skin. In addition, COL17A1-negative cells have poor hemidesmosome function and are not firmly connected to the basement membrane, and are easily extruded into the basal layer by surrounding COL17A1-positive cells. This competition eliminates unhealthy epidermal cells with low levels of COL17A1, leaving healthy cells with high expression of COL17A1, making our skin younger. However, if COL17A1 has too few cells to express and has limited competitive pressure, it will not effectively eliminate those cells that are negative for COL17A1. Overexpression of COL17A1 slows skin aging, but it is obviously unrealistic to do this in human skin, and the researchers turned to compounds that increase the expression of COL17A1. In the end, the researchers found two compounds: Y27632 and apocynin. In vitro, they all increase the expression of COL17A1, allowing epidermal stem cells to grow larger and larger clones. In the body, they also promote wound healing, which has a similar effect to overexpression of COL17A1. According to Nishimura, the author of the paper, the study may eventually develop creams or oral medications to prevent skin aging and promote repair: "We will work with pharmaceutical or cosmetic companies to use these drugs in the clinic." Next, they plan to study the role of similar intercellular competition in aging in organs composed of other epithelial tissues. references: 1. Halberg IB, Lyby K, Wassermann K, et al. Efficacy and safety of oral basal insulin versus subcutaneous insulin glargine in type 2 diabetes: a randomised, double-blind, phase 2 trial[J]. The Lancet Diabetes & Endocrinology, 2019. 2. LIU N, MATSUMURA ​​H, KATO T, et al. Stem cell competition orchestrates skin homeostasis and ageing [J]. Nature, 2019. 3. Kirkwood T. Ageing: too fast by mistake[J]. Nature, 2006, 444(7122): 1015. 4. Nguyen HP, Katta R. Sugar sag: glycation and the role of diet in aging skin [J]. Skin Therapy Lett, 2015, 20(6): 1-5. 5. Langton AK, Halai P, Griffiths CEM, et al. The impact of intrinsic ageing on the protein composition of the dermal-epidermal junction [J]. Mechanisms of ageing and development, 2016, 156: 14-16. 6. Fuchs E. Scratching the surface of skin development[J]. Nature, 2007, 445(7130): 834. 7. Floeth M, Bruckner-Tuderman L. Digenic junctional epidermolysis bullosa: mutations in COL17A1 and LAMB3 genes [J]. The American Journal of Human Genetics, 1999, 65(6): 1530-1537. Half Shell Mussel,Frozen Cooked Half Shell Mussel,Seafood Frozen Half Shell Mussel,Frozen Half Shell Mussel Shengsi Xiangyuan Aquatic Products Co.,Ltd., , https://www.xiangyuan-aquatic.com
Recipe, Shining. But if you want to rely on peach gum for beauty, you can only expect the placebo effect. 
The basement membrane between the epidermis and the dermis 
Knockout of COL17A1 slows wound healing, while overexpression of COL17A1 promotes wound healing 
The older the age, the bigger the color 
Scientists have discovered two drugs that restore the key collagen content of the skin