Title:Tanshinone Alleviates UVA-induced Melanogenesis in Melanocytes via the Nrf2-regulated Antioxidant Defense Signaling Pathway
Volume: 24
Issue: 12
关键词:
UVA，黑色素生成，丹参酮I，二氢丹参酮，Nrf2，抗氧化防御机制。
摘要:
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.
