Lee Jongsung, Jung Kwangseon, Kim Yeong Shik, Park Deokhoon
Biospectrum Life Science Institute, Dangjung Dong, Gunpo City, Gyunggi Do, Republic of Korea.
Life Sci. 2007 Jun 27;81(3):249-54. doi: 10.1016/j.lfs.2007.05.009. Epub 2007 May 24.
An increased level of melanin is characteristic of a large number of skin diseases, including acquired hyperpigmentation conditions such as melasma, post inflammatory melanoderma, and solar lentigo. Thus, there is an increasing need for the development of depigmenting agents. In order to evaluate the depigmenting capacity of diosgenin and elucidate its mechanism of action, several experiments were performed in B16 melanoma cells. Melanin content and Western blots for proteins that are involved in melanogenesis were assessed in this study. The melanin content was significantly inhibited by diosgenin. To clarify the mechanism of the depigmenting property of diosgenin, we examined the involvement of diosgenin in the phosphatidylinositol-3-kinase (PI3K) pathway. In this study, diosgenin inhibited the reduction of Akt and GSK 3beta phosphorylation induced by LY294,002, a PI3K inhibitor. In accordance with this result, production levels of MITF (microphthalmia-associated transcription factor) and tyrosinase were increased by diosgenin. These data suggest that diosgenin inhibits melanogenesis through the activation of the PI3K pathway. This suggestion was further confirmed by the fact that the increased production level of melanin by LY294,002 was reduced by diosgenin in B16 melanoma cells. Our study shows that diosgenin inhibits melanogenesis by activating the PI3K pathway, and also suggests that diosgenin may be an effective inhibitor of hyperpigmentation.
黑色素水平升高是许多皮肤疾病的特征，包括获得性色素沉着疾病，如黄褐斑、炎症后黑皮病和日光性雀斑。因此，对色素脱失剂的需求日益增加。为了评估薯蓣皂苷元的色素脱失能力并阐明其作用机制，在B16黑色素瘤细胞中进行了多项实验。本研究评估了黑色素含量以及参与黑色素生成的蛋白质的蛋白质免疫印迹。薯蓣皂苷元显著抑制了黑色素含量。为了阐明薯蓣皂苷元色素脱失特性的机制，我们研究了薯蓣皂苷元在磷脂酰肌醇-3-激酶（PI3K）途径中的作用。在本研究中，薯蓣皂苷元抑制了PI3K抑制剂LY294,002诱导的Akt和GSK 3β磷酸化的降低。与此结果一致，薯蓣皂苷元提高了小眼相关转录因子（MITF）和酪氨酸酶的产生水平。这些数据表明，薯蓣皂苷元通过激活PI3K途径抑制黑色素生成。薯蓣皂苷元降低了LY294,002在B16黑色素瘤细胞中提高的黑色素产生水平，这一事实进一步证实了这一观点。我们的研究表明，薯蓣皂苷元通过激活PI3K途径抑制黑色素生成，并且还表明薯蓣皂苷元可能是一种有效的色素沉着过度抑制剂。
