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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >ERK Activation by Fucoidan Leads to Inhibition of Melanogenesis in Mel-Ab Cells
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ERK Activation by Fucoidan Leads to Inhibition of Melanogenesis in Mel-Ab Cells

机译：Fucoidan激活ERK导致Mel-Ab细胞黑色素生成受到抑制。

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摘要

Fucoidan, a fucose-rich sulfated polysaccharide derived from brown seaweed in the class Phaeophyceae, has been widely studied for its possible health benefits. However, the potential of fucoidan as a possible treatment for hyperpigmentation is not fully understood. This study investigated the effects of fucoidan on melanogenesis and related signaling pathways using Mel-Ab cells. Fucoidan significantly decreased melanin content. While fucoidan treatment decreased tyrosinase activity, it did not do so directly. Western blot analysis indicated that fucoidan downregulated microphthalmia-associated transcription factor and reduced tyrosinase protein expression. Further investigation showed that fucoidan activated the extracellular signal-regulated kinase (ERK) pathway, suggesting a possible mechanism for the inhibition of melanin synthesis. Treatment with PD98059, a specific ERK inhibitor, resulted in the recovery of melanin production. Taken together, these findings suggest that fucoidan inhibits melanogenesis via ERK phosphorylation.
机译：Fucoidan是富藻糖的一种富含藻糖的硫酸化多糖，来源于褐藻类，属于藻类，已被广泛研究，因为其可能有益健康。然而，岩藻依聚糖作为色素沉着过度可能的治疗方法的潜力尚未得到充分了解。这项研究调查了岩藻依聚糖对Mel-Ab细胞黑色素生成及相关信号通路的影响。岩藻糖聚糖显着降低了黑色素含量。尽管岩藻依聚糖处理降低了酪氨酸酶活性，但并没有直接降低酪氨酸酶的活性。蛋白质印迹分析表明，岩藻依聚糖下调了与小眼症相关的转录因子，并降低了酪氨酸酶蛋白的表达。进一步的研究表明，岩藻依聚糖激活了细胞外信号调节激酶（ERK）途径，提示了抑制黑色素合成的可能机制。用PD98059（一种特殊的ERK抑制剂）进行治疗，可恢复黑色素的产生。两者合计，这些发现表明岩藻依聚糖通过ERK磷酸化抑制黑色素生成。

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