Skin Barrier-Improving and Skin-Soothing Effects of Autophagy-Activating Peptide on Sensitive Skin 

 

Sensitive skin is a widespread condition characterized by unpleasant sensations like stinging, burning, itching, and tingling, triggered by stimuli that do not usually cause such reactions. Impairment of the skin barrier function, heightened inflammatory responses, and altered sensory processing are considered major factors in the pathophysiology of sensitive skin. The stratum corneum, the outermost layer of the skin, acts as a protective barrier, and its dysfunction, often due to imbalances in lipids like ceramides and fatty acids, is associated with sensitive skin. Given the critical role of autophagy in maintaining cellular homeostasis and its potential contribution to epidermal functions, researchers explored the therapeutic potential of an autophagy-activating peptide in addressing sensitive skin syndrome. 

Methods  

The study utilized in vitro and ex vivo human skin explant models to evaluate the effects of pentasodium tetracarboxymethyl palmitoyl didpeptide-12 (PTPD-12) on sensitive skin. Clinical efficacy was assessed in healthy volunteers with sensitive skin. The in vitro studies used cultured human epidermal keratinocytes treated with inflammatory agents. Ex vivo studies used human skin samples exposed to UV radiation. Clinical trials involved measuring trans-epidermal water loss (TEWL) and skin erythema. 

Key Findings 

●Autophagy Activation: Topical application of PTPD-12 increased the expression of LC3 protein in the epidermis of ex vivo human skin, indicating the activation of autophagy. This suggests that PTPD-12 can restore autophagy activity in UV-stressed skin conditions. 

●Anti-Inflammatory Effects: In vitro studies demonstrated that PTPD-12 significantly reduced the secretion of the inflammatory cytokine IL-8 in cultured keratinocytes stimulated by TNF-α or a combination of TNF-α and IL-17A. Ex vivo studies showed that PTPD-12 reduced the expression of TNF-α and PDE4A, inflammatory markers, in UVB-irradiated skin. The ability of PTPD-12 to suppress PDE4A is considered therapeutically significant for inflammatory skin diseases. 

●Skin Barrier Improvement: Ex vivo studies showed that PTPD-12 upregulated the expression of filaggrin and loricrin, which are essential proteins for maintaining epidermal barrier integrity. This indicates that autophagy activation can strengthen a compromised skin barrier. 

●Clinical Efficacy: Clinical trials involving 22 participants identified with sensitive skin showed that after 4 weeks of using a product containing 100 ppm of PTPD-12, there was a significant improvement in skin barrier function (9.73% reduction in TEWL) and a reduction in skin redness (4.23%). These results suggest that the molecular and cellular effects observed in vitro and ex vivo translate to clinical benefits. 

The research is novel in its investigation of autophagy activators as a therapeutic strategy for sensitive skin, addressing the multifactorial nature of the condition. The study highlights the potential of autophagy activation as a promising treatment strategy. Future research should focus on longer-term studies with larger sample sizes to validate these findings and explore other diagnostic tools for sensitive skin. 

Link to the study: https://www.mdpi.com/2079-9284/11/6/223