Jeong Hyo-Soon, Gu Go Eun, Jo Ah Reum, Bang Joon Seok, Yun Hye-Young, Baek Kwang Jin, Kwon Nyoun Soo, Park Kyoung-Chan, Kim Dong-Seok
Department of Biochemistry, Chung-Ang University College of Medicine, 84 Heukseok-ro Dongjak-gu, Seoul 156-756, Republic of Korea.
Graduate School of Clinical Pharmacy, Sookmyung Women's University, Cheongpa-ro 47-gil 100, Youngsan-gu, Seoul 140-742, Republic of Korea.
Eur J Pharmacol. 2015 Aug 15;761:19-27. doi: 10.1016/j.ejphar.2015.04.028. Epub 2015 Apr 29.
Scutellaria baicalensis has been used topically to treat inflammatory skin diseases in traditional East Asian medicine. Because post-inflammatory hyperpigmentation of the skin is difficult to manage, we investigated the effects of baicalin, a major component of S. baicalensis, on melanin synthesis in Mel-Ab cells. Our data showed that baicalin significantly inhibited melanin production and tyrosinase activity in a dose-dependent fashion, but it did not directly influence tyrosinase activity. Moreover, baicalin treatment triggered decreases in both mRNA and protein levels of microphthalmia-associated transcription factor (MITF) and tyrosinase. Although AMP-activated protein kinase (AMPK) and extracellular signal-regulated kinase (ERK) activation were induced in baicalin-treated Mel-Ab cells, they were not responsible for baicalin-induced hypopigmentation. Because the Akt pathway is also known to be involved in regulation of melanogenic protein expression and melanin synthesis, we examined the effects of baicalin on the Akt pathway. Our results showed that baicalin treatment stimulated Akt activation. Treatment with LY294002, a specific Akt inhibitor, restored baicalin-induced melanogenesis inhibition and abolished MITF and tyrosinase downregulation by baicalin. Taken together, our data suggest that Akt activation by baicalin inhibits melanin production via downregulation of MITF and tyrosinase in Mel-Ab cells.
在传统东亚医学中,黄芩已被用于局部治疗炎症性皮肤病。由于皮肤炎症后色素沉着难以处理,我们研究了黄芩的主要成分黄芩苷对Mel-Ab细胞中黑色素合成的影响。我们的数据表明,黄芩苷以剂量依赖性方式显著抑制黑色素生成和酪氨酸酶活性,但它不直接影响酪氨酸酶活性。此外,黄芩苷处理导致小眼畸形相关转录因子(MITF)和酪氨酸酶的mRNA和蛋白质水平均下降。虽然在黄芩苷处理的Mel-Ab细胞中诱导了AMP激活的蛋白激酶(AMPK)和细胞外信号调节激酶(ERK)的激活,但它们与黄芩苷诱导的色素减退无关。由于已知Akt通路也参与黑素生成蛋白表达和黑色素合成的调节,我们研究了黄芩苷对Akt通路的影响。我们的结果表明,黄芩苷处理刺激了Akt激活。用特异性Akt抑制剂LY294002处理可恢复黄芩苷诱导的黑素生成抑制,并消除黄芩苷对MITF和酪氨酸酶的下调作用。综上所述,我们的数据表明,黄芩苷激活Akt通过下调Mel-Ab细胞中的MITF和酪氨酸酶来抑制黑色素生成。