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. 2024;24(12):1529-1539.
doi: 10.2174/0115665240263196230920161019.

Tanshinone Alleviates UVA-induced Melanogenesis in Melanocytes via the Nrf2-regulated Antioxidant Defense Signaling Pathway

Jiaoquan Chen  1 , Zonghao Yin  2 , Nanji Yu  1 , Shanshan Ou  1 , Xue Wang  1 , Huaping Li  1 , Huilan Zhu  1
Affiliations

Tanshinone Alleviates UVA-induced Melanogenesis in Melanocytes via the Nrf2-regulated Antioxidant Defense Signaling Pathway

Jiaoquan Chen et al. Curr Mol Med. 2024.

Abstract

Background: As a complex of natural plant compounds, tanshinone is renowned for its remarkable antioxidant properties. However, the potential impact of tanshinone on melanocyte pigmentation regulation has yet to be elucidated. This study aimed to explore the protective effects of tanshinone I (T-I) and dihydrotanshinone (DHT) on melanogenesis by modulating nuclear factor E2-related factor 2 (Nrf2) signaling and antioxidant defenses in human epidermal melanocyte (HEM) cells.

Methods: HEM cells and Nrf2 knockdown HEM cells were subjected to ultraviolet A (UVA) and treated with T-I and/or DHT. Then, the anti-melanogenic properties of T-I and DHT were examined by assessing tyrosinase activity, melanogenesis-related proteins, and melanin content in UVA-irradiated HEM cells. Furthermore, the antioxidant activities of T-I and DHT were evaluated by assessing oxidant formation and modulation of Nrf2-related antioxidant defenses, including reactive oxygen species (ROS), glutathione (GSH) content, and the activity and expression of antioxidant enzymes, such as catalase (CAT), heme oxygenase-1 (HO-1), and superoxide dismutase (SOD).

Results: Our findings revealed that T-I and DHT diminished melanogenesis in UVAirradiated HEM cells, activated Nrf2-antioxidant response element signaling, and enhanced antioxidant defenses in the irradiated cells. Furthermore, Nrf2 knockdown by shRNA abolished the anti-melanogenesis effects of T-I and DHT on HEM cells against oxidative damage.

Conclusion: These results suggest that T-I and DHT inhibit UVA-induced melanogenesis in HEM cells, possibly through redox mechanisms involving Nrf2 signaling activation and increased antioxidant defenses. This indicates that T-I and DHT have potential as whitening agents in cosmetics and medical treatments for hyperpigmentation disorders.

Keywords: Nrf2; UVA; antioxidant defense mechanism.; dihydrotanshinone; melanogenesis; tanshinone I.

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References

    1. D’Mello S.; Finlay G.; Baguley B.; Askarian-Amiri M.; Signaling pathways in melanogenesis. Int J Mol Sci 2016,17(7),1144 - DOI - PubMed
    1. Rachmin I.; Ostrowski S.M.; Weng Q.Y.; Fisher D.E.; Topical treatment strategies to manipulate human skin pigmentation. Adv Drug Deliv Rev 2020,153,65-71 - DOI - PubMed
    1. Nguyen N.T.; Fisher D.E.; MITF and UV responses in skin: From pigmentation to addiction. Pigment Cell Melanoma Res 2019,32(2),224-236 - DOI - PubMed
    1. Pillaiyar T.; Manickam M.; Jung S.H.; Recent development of signaling pathways inhibitors of melanogenesis. Cell Signal 2017,40,99-115 - DOI - PubMed
    1. Shain A.H.; Bastian B.C.; From melanocytes to melanomas. Nat Rev Cancer 2016,16(6),345-358 - DOI - PubMed

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