دورية أكاديمية
The in vitro and in vivo depigmentation activity of coenzyme Q0, a major quinone derivative from Antrodia camphorata, through autophagy induction in human melanocytes and keratinocytes
العنوان: | The in vitro and in vivo depigmentation activity of coenzyme Q0, a major quinone derivative from Antrodia camphorata, through autophagy induction in human melanocytes and keratinocytes |
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المؤلفون: | You-Cheng Hseu, Jou-Tsen Yeh, Chithravel Vadivalagan, Siang-Jyun Chen, Yugandhar Vudhya Gowrisankar, Sudhir Pandey, Yuan-Tai Hsu, Hung-Rong Yen, Hui-Chi Huang, Jhih-Hsuan Hseu, Hsin-Ling Yang |
المصدر: | Cell Communication and Signaling, Vol 22, Iss 1, Pp 1-21 (2024) |
بيانات النشر: | BMC, 2024. |
سنة النشر: | 2024 |
المجموعة: | LCC:Medicine LCC:Cytology |
مصطلحات موضوعية: | CoQ0, α-MSH, Autophagy, Melanogenesis, Melanin degradation, Medicine, Cytology, QH573-671 |
الوصف: | Abstract Background Coenzyme Q0 (CoQ0), 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. Methods We resolved the depigmenting efficiency of CoQ0 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. Results CoQ0-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, CoQ0 induced antimelanogenesis by suppressing CREB-MITF pathway, tyrosinase expression/activity, and melanin formation via autophagy. TEM data disclosed that CoQ0 increased melanosome-engulfing autophagosomes and autolysosomes in α‐MSH-stimulated B16F10 cells. CoQ0-inhibited melanogenesis in α‐MSH-stimulated B16F10 cells was reversed by pretreatment with the autophagy inhibitor 3-MA or silencing of LC3. Additionally, CoQ0-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, CoQ0 induced melanin degradation by suppressing melanosome gp100 and melanin formation via autophagy. TEM confirmed that CoQ0 increased melanosome-engulfing autophagosomes and autolysosomes in melanin-feeding HaCaT cells. Treatment with 3-MA reversed CoQ0-mediated melanin degradation in melanin-feeding HaCaT cells. In vivo study showed that CoQ0 suppressed endogenous body pigmentation by antimelanogenesis and melanin degradation through autophagy induction in a zebrafish model. Conclusions Our results showed that CoQ0 exerted antimelanogenesis and melanin degradation by inducing autophagy. CoQ0 could be used in skin-whitening formulations as a topical cosmetic application. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1478-811X |
Relation: | https://doaj.org/toc/1478-811X |
DOI: | 10.1186/s12964-024-01537-6 |
URL الوصول: | https://doaj.org/article/7be9207b94f347068f610f2e4e62afe6 |
رقم الأكسشن: | edsdoj.7be9207b94f347068f610f2e4e62afe6 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 1478811X |
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DOI: | 10.1186/s12964-024-01537-6 |