[Afrisil Speciality Ingredients]
THE SKIN DRYNESS INHIBITORY MECHANISM OF GO-VC, AN AMPHIPHILIC ASCORBIC-ACID DERIVATIVE Since tight junctions are known to play an important role in skin barrier function, their functional deterioration is thought to induce skin dryness. Provitamin, represented locally by Afrisil Speciality Ingredients, has investigated the skin dryness-inhibitory effect of GO-VC with a focus on tight junctions.
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scorbic-acid (AsA) derivatives are widely used in cosmetics for their skin-brightening, anti-wrinkle and anti-acne effects. However, since AsA and its derivatives are reported to suppress the secretion of sebum1, they have a possibility to promote skin dryness in some cases. In recent years, 2-O-glyceryl-3-O-octyl ascorbic acid (GO-VC), of which glycerine and octanol are bound to hydroxyl groups at the C-2 and C-3 positions of AsA respectively (see Figure 1), has been developed as an amphiphilic AsA derivative with excellent stability. Since glycerine and octanol are known to have humectant ability and antimicrobial activity, GO-VC is anticipated to have a moisturising effect and antimicrobial activity. In a clinical study, GO-VC has been confirmed to have a suppressing effect on Propionibacterium acnes proliferation and to improve Acne vulgaris. Regarding the moisturising effect, a sensory evaluation confirmed that GO-VC provides skin with a moist feeling that is not sticky or greasy (see Figure 2). However, the skin dryness-inhibitory effect and the mechanism of action of GO-VC were still unclear. Provitamin conducted various studies on human volunteers and epidermal keratinocytes in order to clarify the skin dryness-inhibitory effect and GO-VC mechanism of action. The results of this study were presented by Provitamin’s researchers at the 2020 IFSCC Congress in Yokohama, Japan.
Figure 1: Chemical structure of GO-VC
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Figure 2: Sensory evaluation test of GO-VC
What are tight junctions? Existing as an outermost layer, the skin is the organ responsible for barrier protection as it prevents water loss and protects the body from the invasion of external chemicals and microorganisms. The skin barrier function mainly originates from its lipid lamella structure consisting of ceramides, cholesterol and fatty acids that are found in the interstice of the stratum corneum (SC) and tight junctions (TJ), which exist at the second level of the granular layer.2, 3, 4 TJ is one of the cell adhesion apparatuses consisting of several proteins such as claudin-1, occludin and zonula occludens-1 (ZO-1) (see Figure 3). Although the important function of TJ is recognised as its barrier protection property against the penetration of metal ions such as Ca2+ and Mg2+ between SC and the granular layer4, TJ is also known to function as a barrier against water. For instance, atopic dermatitis – a chronic inflammatory disease as a result of impaired barrier function – is reported to show the dysfunction of TJ due to the down-regulation of claudin-1 expression.5 Even in healthy skin, reduced barrier function can result in a rough texture and the start of skin
