2/2022
vol. 39
abstract:
Original paper
Effects of tea polyphenols on UVA-induced
melanogenesis via inhibition of α-MSH-MC1R signalling
pathway
1.
Department of Dermatology, Guangzhou Institute of Dermatology, Guangzhou, Guangdong, China
Adv Dermatol Allergol 2022; XXXIX (2): 327-335
Online publish date: 2022/05/09
Introduction and aim Ultraviolet (UV) irradiation is a major environmental factor affecting photoaging, which is characterized by skin wrinkle formation and hyperpigmentation. Although many factors are involved in the melanogenesis progress, UV is thought to play a major role in tanning. The pathway of a-melanocyte-stimulating hormone (a-MSH)-melanocortin receptor 1 (MC1R) is associated with UV-induced melanogenesis. Thus, a-MSH antagonists may have applications in the prevention of melanogenesis.
Aim: To investigate the effects of tea polyphenols (TPS) on pigmentation, and further explore the underlying mechanism.
Material and methods Human keratinocyte cell line (HaCaT) cells and Human epidermal melanocytes (HEM) were exposed to UVA and treated with different concentrations of TPS or Nonapeptide-1 acetate salt (N-1A). Then, cell viability, melanin content, and tyrosinase activity of both kinds of cells were detected. Quantification of a-MSH in HaCaT cells and HEM cells determined by ELISA assays. Immunohistochemistry of HEM cells was employed to further investigate the expression of melanogenesis-related proteins.
Results The different concentrations of TPS were found to decrease the melanin content, tyrosinase activity and melanogenesis-related proteins such as microphthalmia-associated transcription factor (MITF), tyrosinase-related protein (TRP)1, and TRP2. Besides, TPS inhibited a-MSH-MC1R signalling through directly suppressed a-MSH expression rather than the down-regulated expression level of MC1R.
Conclusions Our findings indicate that TPS may be a potential whitening agent for use in cosmetics and the medical treatment of hyperpigmentation disorders.
keywords:
UV, melanogenesis, tea polyphenols, a-MSH-MC1R
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