A formulation containing the combination of niacinamide + TXA reduced the appearance of irregular pigmentation, providing an effect beyond that achieved with sunscreen.

BackgroundOver the last decade, the incidence of ultraviolet B (UVB)-related skin problems has increased. Oxidative stress caused by UVB induces the secretion of melanocyte growth and activating factors from keratinocytes, which results in the formation of cutaneous hyperpigmentation. Therefore, increasing the antioxidant abilities of skin cells is thought to be a beneficial strategy for the development of sunscreen agents. Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that is known to exhibit antioxidant properties.ObjectiveThe purpose of this study was to investigate the effect of SOD1 on alpha-melanocyte stimulating hormone (α-MSH) and UVB-induced melanogenesis in B16F10 melanoma cells and HRM-2 melanin-possessing hairless mice.MethodsThe inhibitory effect of SOD1 on tyrosinase activity was evaluated in a cell-free system. Additional experiments were performed using B16F10 melanoma cells to demonstrate the effects of SOD1 in vitro, and HRM-2 melanin-possessing hairless mice were used to evaluate the antimelanogenic effects of SOD1 in vivo.ResultsWe found that SOD1 inhibited melanin production in a dose-dependent manner without causing cytotoxicity in B16F10 melanoma cells. SOD1 did not inhibit tyrosinase activity under cell-free conditions. The results indicate that SOD1 may reduce pigmentation by an indirect, nonenzymatic mechanism. We also found that SOD1 decreased UVB-induced melanogenesis in HRM-2 melanin-possessing hairless mice, as visualized through hematoxylin and eosin staining and Fontana-Masson staining.ConclusionOur results indicate that SOD1 has an inhibitory effect on α-MSH and UVB-induced melanogenesis, indicating that SOD1 may be a promising sunscreen agent.

Topical application of human growth factor and hyaluronic acid was beneficial in reducing periorbital wrinkles.

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Saururus chinensis has been used in folk medicine in Korea for the treatment of edema, jaundice, gonorrhea, and several inflammatory diseases. Saururi chinensis extracts (SCE) have demonstrated antiinflammatory and anti-oxidant activities, as well as anti-asthmatic, antihypertensive, anti-angiogenic, and therapeutic activities for atopic dermatitis. However, the inhibitory activity of SCE on the melanogenesis signaling pathway is not completely understood. This study examined the effects of SCE on the melanogenesis signaling pathway activated by α-melanocyte-stimulating hormone (α-MSH). We found that SCE inhibited melanin production in a dose-dependent manner without causing cytotoxicity in B16F10 cells. Interestingly, SCE decreased α-MSH-induced tyrosinase activity in B16F10 cells but did not inhibit tyrosinase activity under cell-free conditions. The results of this study indicate that SCE may reduce pigmentation by way of an indirect, nonenzymatic mechanism. We also found that SCE decreased α-MSH-induced microphthalmiaassociated transcription factor (MITF) and tyrosinase expression and induced the activation of extracellular signal-regulated kinase (ERK). These results suggest that the depigmenting effect of SCE may result from downregulation of MITF and tyrosinase expression due to increased ERK activity. Thus, our results provide evidence that SCE might be useful as a potential skin-whitening agent.Key words B16F10 melanoma cell; extracellular signal-regulated kinase; melanogenesis; Saururi chinensis; tyrosinase In mammals, pigmentation results from the synthesis and distribution of melanin in the skin, hair bulbs and eyes. Melanin is a pigmented polymer, which provides photoprotection to the skin against UV radiation. Various hyperpigmented disorders such as melasma can be caused by excessive synthesis of melanin. Melanogenesis comprises many enzymatic oxidation steps in which tyrosine is converted to eumelanin and pheomelanin.1) Tyrosinase, tyrosinase-related protein-1 (TRP-1), and dihydroxyphenylalaminechrome tautomerase (TRP-2) are key enzymes involved in the regulation of melanogenesis.2)The expressions of tyrosinase and TRP1 and TRP2 genes are activated by microphthalmia-associated transcription factor (MITF) through cooperation with protein kinase C (PKC). 3)Tyrosinase catalyses the rate-limiting reaction of the melanogenic process, and melanin production is regulated mainly by the expression and activation of tyrosinase. [3][4][5] Recently, the inhibition of extracellular signal-regulated kinase (ERK) signaling was reported to induce hyperpigmentation by increasing tyrosinase activity, suggesting that the activation of ERK signaling downregulates melanogenesis by inhibiting tyrosinase activity. [6][7][8] These reports show that the improved methods of melanogenesis inhibition do not suppress the activity of tyrosinase as much as they control the tyrosinase upstream signaling pathway related to its activation and expression.Several known natural melanin synthesis inhibitors, including arbutin and koj...