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Báo cáo y học: "Antimelanogenic effect of c-phycocyanin through modulation of tyrosinase expression by upregulation of ERK and downregulation of p38 MAPK signaling pathway"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Antimelanogenic effect of c-phycocyanin through modulation of tyrosinase expression by upregulation of ERK and downregulation of p38 MAPK signaling pathways. | Wu et al. Journal of Biomedical Science 2011 18 74 http www.jbiomedsci.eom content 18 1 74 NSC The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Antimelanogenic effect of c-phycocyanin through modulation of tyrosinase expression by upregulation of ERK and downregulation of p38 MAPK signaling pathways Li-Chen Wu1 2 Yu-Yun Lin2 Szu-Yen Yang2 Yu-Ting Weng2 and Yi-Ting Tsai2 Abstract Background Pigmentation is one of the essential defense mechanisms against oxidative stress or UV irradiation however abnormal hyperpigmentation in human skin may pose a serious aesthetic problem. C-phycocyanin Cpc is a phycobiliprotein from spirulina and functions as an antioxidant and a light harvesting protein. Though it is known that spirulina has been used to reduce hyperpigmentation little literature addresses the antimelanogenic mechanism of Cpc. Herein we investigated the rationale for the Cpc-induced inhibitory mechanism on melanin synthesis in B16F10 melanoma cells. Methods Cpc-induced inhibitory effects on melanin synthesis and tyrosinase expression were evaluated. The activity of MAPK pathways-associated molecules such as MAPK ERK and p38 MAPK were also examined to explore Cpc-induced antimelanogenic mechanisms. Additionally the intracellular localization of Cpc was investigated by confocal microscopic analysis to observe the migration of Cpc. Results Cpc significantly P 0.05 reduced both tyrosinase activity and melanin production in a dose-dependent manner. This phycobiliprotein elevated the abundance of intracellular cAMP leading to the promotion of downstream ERK1 2 phosphorylation and the subsequent MITF the transcription factor of tyrosinase degradation. Further Cpc also suppressed the activation of p38 causing the consequent disturbed activation of CREB the transcription factor of MITF . As a result Cpc negatively regulated tyrosinase gene expression resulting in the