Department of Microbiology, Pusan National University, Busan, Republic of Korea.
Int J Mol Med. 2012 Jan;29(1):119-24. doi: 10.3892/ijmm.2011.807. Epub 2011 Oct 3.
Cordycepin has been a traditional medicine in China and Korea for centuries. This study explored the inhibitory effect of cordycepin on melanogenesis and the relative molecular mechanisms. Cordycepin inhibited melanin synthesis-related enzymes, such as tyrosinase, tyrosinase-related protein-1 (TRP1) and tyrosinase-related protein-2 (TRP2). α-MSH and IBMX were reported as melanin synthesis enhancers. Both of them could increase intracellular melanin synthesis by activation of the microphthalmia-associated transcription factor (MITF) signaling pathway. In the MITF pathway, the phosphorylation of cAMP related binding protein (CREB) activated the transcription of MITF, resulting in increasing melanin synthesis. Cordycepin also decreased the phosphorylation of CREB induced by α-MSH and IBMX in B16F10 melanoma cells. Accordingly, cordycepin inhibited melanogenesis signaling pathways by activating ERK and AKT signaling pathways to regulate the suppression of MITF and its downstream pathways including tyrosinase, TRP1 and TRP2. These results indicate the role of cordycepin as a potent depigmenting agent for cosmetics.
蛹虫草素在中国和韩国已被作为传统药物使用了数个世纪。本研究探索了蛹虫草素对黑色素生成的抑制作用及其相关的分子机制。蛹虫草素抑制了黑色素合成相关的酶，如酪氨酸酶、酪氨酸酶相关蛋白-1（TRP1）和酪氨酸酶相关蛋白-2（TRP2）。α-MSH 和 IBMX 被报道为黑色素合成促进剂。它们都可以通过激活小眼畸形相关转录因子（MITF）信号通路来增加细胞内黑色素的合成。在 MITF 信号通路中，cAMP 相关结合蛋白（CREB）的磷酸化激活 MITF 的转录，从而增加黑色素的合成。蛹虫草素还降低了 α-MSH 和 IBMX 在 B16F10 黑色素瘤细胞中诱导的 CREB 磷酸化。因此，蛹虫草素通过激活 ERK 和 AKT 信号通路来抑制 MITF 及其下游途径，包括酪氨酸酶、TRP1 和 TRP2 的表达，从而抑制黑色素生成信号通路。这些结果表明蛹虫草素作为一种有效的化妆品美白剂的作用。
