Persicaria tinctoria Extract Mitigates UV-Associated DNA Damage and Inflammation, While Boosting Vitamin D3 and Melanin in Human Skin

Benefit/risk management of skin exposure to sunlight, especially ultraviolet (UV) rays, is mainly driven by photoaging, cancer incidence, and the requirement for vitamin D3 synthesis. Antioxidant phytocompounds are considered to be a valuable source of molecules to protect skin from UV-induced damage, but their impact on other UV-related metabolic pathways is rarely described. In this study, an indigoid-rich Persicaria tinctoria extract (PTE) was evaluated on three consequences of UV exposure: DNA damage and inflammation, vitamin D3 content, and melanogenesis. A moderate UV exposure was applied on skin models, corresponding to approximately 1 h exposure in the spring in western Europe. UV-induced DNA damage and inflammation were measured through the quantification of cyclobutane pyrimidine dimers (CPDs) and cytokines. Response to heat stress was quantified through the release of prostaglandin. Then, the impact of PTE on vitamin D3 and melanin synthesis was observed. PTE decreased by −56% in the number of cells presenting CPDs. PTE decreased the production of pro-inflammatory cytokine IL-6 (−59%) and stimulated the release of the protective cytokine IL-1Ra (+49%). It decreased PGE2 release by −27%. In skin explants, PTE boosted the vitamin D3 concentration (+345%). Several genes involved in melanogenesis were up-regulated by PTE (MC1R × 2.46, MITF × 1.69, TYR × 2.06, MLPH × 1.53). It promoted melanin content by +126% and by +86% when associated with SPF 30. The extract decreased the amount of protective eumelanin, leading to visible skin tanning of reconstructed human epidermis (L*-15%, ITA −125%). As a new finding, PTE minimized DNA damage and inflammation caused by a daily dose of UV, and surprisingly, promoted vitamin D3 and eumelanin synthesis, suggesting that it represents an opportunity to reconcile skin protection and the physiological need for sunlight.