The anti-melanogenesis, anti-photoaging, and anti-inflammation of coenzyme Q0, a major quinone derivative from Antrodia camphorata, through antioxidant Nrf2 signaling pathways in UVA/B-irradiated keratinocytes

Abstract

We discovered that Coenzyme Q0 (CoQ0), a major quinone derivative from Antrodia camphorata, exerts antimelanogenic, antiphotoaging, and anti-inflammatory effects by activating Nrf2-mediated antioxidant pathways on UVA (3 or 10 J/cm2)/UVB (80 mJ/cm2)-irradiated keratinocyte (HaCaT) cells. CoQ0 downregulated p53/POMC-mediated α-MSH expression in UVA (3 J/cm2)-irradiated HaCaT cells. Additionally, conditioned medium (containing α-MSH) derived from CoQ0-pretreated and UVA-irradiated HaCaT cells inhibited melanogenesis and melanin generation in melanoma B16F10 cells. CoQ0 enhanced Nrf2 nuclear translocation, resulting in antioxidant HO-1, γ-GCLC, and NQO-1 expression in HaCaT cells. Silencing of Nrf2 reversed CoQ0-inhibited ROS (H2O2) and α-MSH expression in UVA (3 J/cm2)-irradiated HaCaT cells. Furthermore, CoQ0 exerted antiphotoaging by activating Nrf2 pathway, leading to the inhibition of ROS-mediated apoptosis in UVA (10 J/cm2)-irradiated HaCaT cells. CoQ0 ameliorated UVB (80 mJ/cm2)-induced ROS-mediated inflammation (NFκB, iNOS, and COX-2 levels) by activating Nrf2 pathway in HaCaT cells. CoQ0 could be used in formulations as a topical cosmetic application.

Keywords

• Antrodia camphorata
• CoQ0
• UVA/B
• α-MSH
• ROS
• Nrf2