Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung 40402, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan; Chinese Medicine Research Center, China Medical University, Taichung 40402, Taiwan; Research Center of Chinese Herbal Medicine, China Medical University, Taichung 40402, Taiwan.
Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung 40402, Taiwan.
Biochem Pharmacol. 2019 Jun;164:299-310. doi: 10.1016/j.bcp.2019.04.015. Epub 2019 Apr 13.
Coenzyme CoQ10 (CoQ10), a ubiquinone compound, has been reported to inhibit tyrosinase activity and melanin production in melanoma B16F10 cells. However, the molecular mechanism underlying this inhibitory effect is poorly understood. In this paper we aimed to investigate the molecular mechanisms involved in the anti-melanogenic activity of CoQ10 (1-2 μM) in UVA (5 J/cm)-irradiated keratinocyte HaCaT cells and α-MSH stimulated B16-F10 cells. It was observed that CoQ10 suppressed p53/POMC, α-MSH production as well as inhibited ROS generation in UVA-irradiated keratinocyte HaCaT cells. CoQ10 down-regulated the melanin synthesis in α-MSH-stimulated B16-F10 cells by suppressing the MITF expression by down regulating the cAMP mediated CREB signaling cascades. Furthermore, in vivo evidence demonstrated the inhibitory effect of CoQ10 on endogenous pigmentation in zebrafish. Increased nuclear Nrf2 translocation accompanied by the induction of HO-1 and γ-GCLC genes were observed in CoQ10 treated keratinocyte HaCaT cells. Notably, silencing of Nrf2 (siRNA transfection) significantly diminished CoQ10-mediated anti-melanogenic activity, as evidenced by impaired antioxidant HO-1 gene, uncontrolled ROS generation, and α-MSH production following UVA irradiation. To conclude, CoQ10 is an effective de-pigmention or skin-whitening agent and could be used in cosmetics for topical application.
辅酶 Q10（CoQ10）是一种泛醌化合物，据报道可抑制黑色素瘤 B16F10 细胞中的酪氨酸酶活性和黑色素生成。然而，这种抑制作用的分子机制尚不清楚。在本文中，我们旨在研究 CoQ10（1-2 μM）在 UVA（5 J/cm）照射角质形成细胞 HaCaT 细胞和 α-MSH 刺激 B16-F10 细胞中抗黑色素生成活性的分子机制。结果表明，CoQ10 抑制了 p53/POMC、α-MSH 的产生，并抑制了 UVA 照射的角质形成细胞 HaCaT 细胞中 ROS 的产生。CoQ10 通过下调 cAMP 介导的 CREB 信号级联来抑制 MITF 表达，从而下调 α-MSH 刺激的 B16-F10 细胞中的黑色素合成。此外，体内证据表明 CoQ10 对斑马鱼内源性色素沉着的抑制作用。在 CoQ10 处理的角质形成细胞 HaCaT 细胞中观察到核 Nrf2 易位增加，同时诱导 HO-1 和 γ-GCLC 基因表达。值得注意的是，Nrf2 沉默（siRNA 转染）显著减弱了 CoQ10 介导的抗黑色素生成活性，这表现在抗氧化 HO-1 基因受损、UVA 照射后 ROS 失控产生和 α-MSH 产生。总之，CoQ10 是一种有效的褪色或美白剂，可用于化妆品的局部应用。
