Mushroom extract recovers youthful skin properties

 It boosts skin metabolism under stress induced by nutrient deficiency and increases the skin’s defense against oxidative stress. In addition, by stimulating different collagens of the dermis and DEJ, the AI compensates the age-related decrease in collagen level. At the same time a correctly structured network of collagens and a high quality DEJ and dermis are stimulated. As a result, skin elasticity and firmness are increased. The newly synthesised collagens act as endogenous fillers, plumping up the skin from the inside, resulting in a smoother, and more youthful looking skin. The organism is daily aggressed by different types of stress. The best known is oxidative stress defined as the toxic effect of chemically reactive oxygen species (ROS) or reactive nitrogen species. Reactive oxygen species (ROS) can damage cellular components, leading to impaired physiological functions and thus inducing ageing.1,2 To counteract ROS, cells have many anti-oxidant enzyme systems. Among these, peroxiredoxins, are key enzymes having a role in cellular detoxification due to their reduction potential: they catalyse the conversion of molecules from their oxidised (harmful) form to their reduced (non-toxic) form. During this process of detoxification, peroxiredoxins themselves are oxidised and must therefore be regenerated to be effective again.3 Two enzymatic systems participate in the regeneration of peroxiredoxins: the thioredoxin/thioredoxin reductase 1 (TXNRD1) couple and sulfiredoxin (SRXN1). If peroxiredoxins are weakly oxidised the thioredoxin/TXNRD1 couple is effective enough. However, if oxidation is too strong a system including SRXN1 and the thioredoxin/TXNRD1 couple is put in place.4 Thanks to their detoxifying potential, SRXN1 and TXNRD1 allow the regeneration of peroxiredoxins, key enzymes to fight against the ROS and their deleterious effects. The term “adaptogen” refers to the potential of an active to improve the capacity of an organism to fight against any kind of stress. In consequence, an active with an adaptogen effect may be able to increase stress resistance of cells.

Skin collagens

More than 80% of the skin is constituted by collagens. Different types of cutaneous collagen are described: fibrillar collagens, reticular collagens and FACITs (fibrilassociated collagens with interrupted triple helix)5 (Fig. 2). All these collagens are expressed at different levels in the skin. Besides the well known type I and type III collagens present in major quantity, the dermis also contains quantitatively minor collagens, including type V, XII or XVI collagens.5 The fibrillar type V collagen plays an important role in the type I collagen fibre initiation and size control. It interacts with the core of on-growing type I collagen fibrils to favour the fibre formation, and its globular domains induce a steric constraint that limits the lateral growth of collagen fibres and so regulates their diameter.6,7,8 Types XII and XVI collagens are FACITs that adopt a specific structure, like a trident, to interact with and to organise the different collagen fibres of the extra-cellular matrix (ECM).9,10 The type XII and XVI collagens are mainly located in papillary dermis and are important for the quality of the ECM. In the dermo-epidermal junction (DEJ), specific collagens are also present, produced by keratinocytes and/or fibroblasts. The main collagen in the DEJ is the type IV collagen forming a network on which different components of epidermis or dermis are anchored, to assume an efficient cohesion of these two skin layers.11 A collagen specific of basal membranes, present in DEJ, is the type XVIII collagen belonging to the multiplexin family, adopting a structure similar to FACIT.12,13 With age, destruction of existing collagen and failure to replace damaged collagen with newly synthesised material are central to the deleterious changes observed in aged/photoaged dermis, inducing decrease of skin firmness.14 In addition, with ageing the skin becomes more fragile with a decrease of the cohesion between epidermis and dermis, due to an alteration of the structure of the DEJ.