Abstract
Madecassoside (MA), a pentacyclic triterpene isolated from Centella asitica (L.), is used as a therapeutic agent in wound healing and also as an anti-inflammatory and anti-aging agent. However, the involvement of MA in skin-pigmentation has not been reported. This study was conducted to investigate the effects of MA on ultraviolet (UV)-induced melanogenesis and mechanisms in a co-culture system of keratinocytes and melanocytes. MA significantly inhibited UVR-induced melanin synthesis and melanosome transfer in the co-culture system. These effects were further demonstrated by the MA-induced inhibition of protease-activated receptor-2 expression and its signaling pathway, cyclooxygenase-2, prostaglandin E2 and prostaglandin F2 alpha in keratinocytes. The clinical efficacy of MA was confirmed on artificially tanned human skin. MA significantly reduced UV-induced melanin index at 8 weeks after topical application. Overall, the study demonstrated significant benefits of MA use in the inhibition of hyperpigmentation caused by UV irradiation.
Highlights
In mammals, pigmentation results from the synthesis and distribution of melanin in the skin, hair bulbs, and eyes
To determine whether MA reduces UVB-induced melanin synthesis in the keratinocyte/melanocyte co-culture system, melanin contents were measured during co-culture
After HaCaT keratinocytes in the upper chamber were irradiated with UVB, MA were added to the indicated concentration and placed above the melanocytes
Summary
Pigmentation results from the synthesis and distribution of melanin in the skin, hair bulbs, and eyes. Prostaglandin (PG) is a lipid signaling intermediate produced by cyclooxygenation of arachidonic acid through the action of cyclooxygenase (COX) enzymes and prostaglandin E2 (PGE2). PGE2 and prostaglandin F2α (PGF2α) are the main PGs produced by keratinocytes in response to UV irradiation. Several reports have suggested that PGs mediate postinflammatory pigmentary changes by modulating melanin synthesis and melanocyte dendricity [3,4,5]. PAR-2 has been linked to the upregulation of COX-2 and the release of arachidonic acid and secretion of PGE2 and PGF2α [10,11]. Several reports have suggested that PAR-2 mediates cutaneous pigmentation through increased uptake of melanosomes by keratinocytes and by the release of PGE2 and PGF2α that stimulate melanocyte dendricity [12]. We examined the the effects of MA on UVR-induced melanogenesis and its mechanisms of action in a co-culture system of keratinocytes and melanocytes
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