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二十二碳六烯酸通过增加酪氨酸酶降解来抑制体外培养的小鼠黑色素瘤细胞中的黑色素合成。

Docosahexaenoic acid inhibits melanin synthesis in murine melanoma cells in vitro through increasing tyrosinase degradation.

作者信息

Balcos Marie Carmel, Kim Su Yeon, Jeong Hyo-soon, Yun Hye-young, Baek Kwang Jin, Kwon Nyoun Soo, Park Kyoung-chan, Kim Dong-seok

机构信息

Department of Biochemistry, Chung-Ang University College of Medicine, 221 Heukseok-dong, Dongjak-gu, Seoul 156-756, Korea.

Department of Dermatology, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-si, Kyoungki-do 463-707, Korea.

出版信息

Acta Pharmacol Sin. 2014 Apr;35(4):489-95. doi: 10.1038/aps.2013.174. Epub 2014 Feb 24.

Abstract

AIM

To investigate the effects of docosahexaenoic acid (DHA) on melanin synthesis and related regulatory mechanisms.

METHODS

B16F10 mouse melanoma cells were exposed to DHA for 3 d, and melanin content and tyrosinase activity were measured. Western blot analysis was used to analyze the protein levels in DHA-mediated signal transduction pathways.

RESULTS

DHA (1-25 μmol/L) did not affect the viability of B16F10 cells, but decreased α-MSH-induced melanin synthesis in a concentration-dependent manner. DHA concentration-dependently reduced tyrosinase activity in the cells, but did not affect mushroom tyrosinase activity in a cell-free system. Furthermore, DHA treatment significantly reduced tyrosinase level without affecting microphthalmia-associated transcription factor (MITF) in the cells. DHA did not activate ERK and Akt in the cells. Pretreatment with the proteasome inhibitor MG132 (80 nmol/L) abolished DHA-induced tyrosinase reduction.

CONCLUSION

DHA inhibits melanogenesis in B16F10 cells in vitro through increasing tyrosinase degradation. The results suggest that DHA may be a potential agent for treatment of hyperpigmentary disorders of skin.

摘要

目的

研究二十二碳六烯酸(DHA)对黑色素合成及相关调控机制的影响。

方法

将B16F10小鼠黑色素瘤细胞暴露于DHA中3天,检测黑色素含量和酪氨酸酶活性。采用蛋白质免疫印迹分析(Western blot分析)来分析DHA介导的信号转导通路中的蛋白质水平。

结果

DHA(1 - 25 μmol/L)不影响B16F10细胞的活力,但以浓度依赖的方式降低α - 促黑素(α - MSH)诱导的黑色素合成。DHA浓度依赖性地降低细胞中的酪氨酸酶活性,但不影响无细胞体系中蘑菇酪氨酸酶的活性。此外,DHA处理显著降低细胞中酪氨酸酶水平,但不影响小眼相关转录因子(MITF)。DHA未激活细胞中的细胞外信号调节激酶(ERK)和蛋白激酶B(Akt)。用蛋白酶体抑制剂MG132(80 nmol/L)预处理可消除DHA诱导的酪氨酸酶减少。

结论

DHA通过增加酪氨酸酶降解在体外抑制B16F10细胞中的黑色素生成。结果表明,DHA可能是治疗皮肤色素沉着过度性疾病的潜在药物。

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