Department of Cosmeceutics, College of Pharmacy, China Medical University, Taichung, 406040, Taiwan.
Chinese Medicine Research Center, China Medical University, Taichung, 406040, Taiwan.
Cell Commun Signal. 2024 Feb 26;22(1):151. doi: 10.1186/s12964-024-01537-6.
Coenzyme Q (CoQ), a novel quinone derivative of Antrodia camphorata, has been utilized as a therapeutic agent (including antioxidant, anti-inflammatory, antiangiogenic, antiatherosclerotic, and anticancer agents); however, its depigmenting efficiency has yet to be studied.
We resolved the depigmenting efficiency of CoQ through autophagy induction in melanoma (B16F10) and melanin-feeding keratinocyte (HaCaT) cells and in vivo Zebrafish model. Then, MPLC/HPLC analysis, MTT assay, Western blotting, immunofluorescence staining, LC3 transfection, melanin formation, GFP-LC3 puncta, AVO formation, tyrosinase activity, and TEM were used.
CoQ-induced autophagy in B16F10 cells was shown by enhanced LC3-II accumulation, ATG7 expression, autophagosome GFP-LC3 puncta, and AVOs formation, and ATG4B downregulation, and Beclin-1/Bcl-2 dysregulation. In α-MSH-stimulated B16F10 cells, CoQ induced antimelanogenesis by suppressing CREB-MITF pathway, tyrosinase expression/activity, and melanin formation via autophagy. TEM data disclosed that CoQ increased melanosome-engulfing autophagosomes and autolysosomes in α-MSH-stimulated B16F10 cells. CoQ-inhibited melanogenesis in α-MSH-stimulated B16F10 cells was reversed by pretreatment with the autophagy inhibitor 3-MA or silencing of LC3. Additionally, CoQ-induced autophagy in HaCaT cells was revealed by enhanced LC3-II accumulation, autophagosome GFP-LC3 puncta and AVO formation, ATG4B downregulation, ATG5/ATG7 expression, and Beclin-1/Bcl-2 dysregulation. In melanin-feeding HaCaT cells, CoQ induced melanin degradation by suppressing melanosome gp100 and melanin formation via autophagy. TEM confirmed that CoQ increased melanosome-engulfing autophagosomes and autolysosomes in melanin-feeding HaCaT cells. Treatment with 3-MA reversed CoQ-mediated melanin degradation in melanin-feeding HaCaT cells. In vivo study showed that CoQ suppressed endogenous body pigmentation by antimelanogenesis and melanin degradation through autophagy induction in a zebrafish model.
Our results showed that CoQ exerted antimelanogenesis and melanin degradation by inducing autophagy. CoQ could be used in skin-whitening formulations as a topical cosmetic application.
辅酶 Q（CoQ）是一种新型的茵陈二炔类衍生物，已被用作治疗剂（包括抗氧化剂、抗炎剂、抗血管生成剂、抗动脉粥样硬化剂和抗癌剂）；然而，其美白效率尚未得到研究。
我们通过在黑色素瘤（B16F10）和黑色素喂养角质形成细胞（HaCaT）细胞以及体内斑马鱼模型中诱导自噬来解决 CoQ 的美白效率问题。然后，使用 MPLC/HPLC 分析、MTT 测定、Western blot、免疫荧光染色、LC3 转染、黑色素形成、GFP-LC3 斑点、AVO 形成、酪氨酸酶活性和 TEM。
CoQ 在 B16F10 细胞中诱导自噬，表现为 LC3-II 积累增加、ATG7 表达增加、自噬体 GFP-LC3 斑点和 AVO 形成增加以及 ATG4B 下调和 Beclin-1/Bcl-2 失调。在 α-MSH 刺激的 B16F10 细胞中，CoQ 通过抑制 CREB-MITF 通路、酪氨酸酶表达/活性和黑色素形成来诱导抗黑色素生成。TEM 数据显示，CoQ 增加了 α-MSH 刺激的 B16F10 细胞中黑素体吞噬自噬体和自溶体。在 α-MSH 刺激的 B16F10 细胞中，CoQ 抑制黑色素生成可被自噬抑制剂 3-MA 预处理或 LC3 沉默逆转。此外，CoQ 在 HaCaT 细胞中诱导的自噬作用通过增强 LC3-II 积累、自噬体 GFP-LC3 斑点和 AVO 形成、ATG4B 下调、ATG5/ATG7 表达和 Beclin-1/Bcl-2 失调来揭示。在黑色素喂养的 HaCaT 细胞中，CoQ 通过抑制黑素体 gp100 和黑色素形成来诱导黑色素降解，从而诱导自噬。TEM 证实 CoQ 增加了黑色素喂养的 HaCaT 细胞中黑素体吞噬的自噬体和自溶体。用 3-MA 处理可逆转 CoQ 介导的黑色素喂养的 HaCaT 细胞中黑色素的降解。体内研究表明，CoQ 通过在斑马鱼模型中诱导自噬来抑制内源性身体色素沉着，从而发挥抗黑色素生成和黑色素降解作用。
我们的结果表明，CoQ 通过诱导自噬发挥抗黑色素生成和黑色素降解作用。CoQ 可作为局部化妆品应用于美白制剂中。
Zotero 插件
