To date, there is no report about the effect of Lycium chinense Miller root SFE on melanin production. This is the first study to evidence the potential inhibitory effect of Lycium chinense Miller root SFE on melanogenesis in B16F10 melanoma cells. In addition, the root extract also shows antioxidant capaci ties, which sellekchem fits the trend of skin anti hyperpigmentation agents that show dual functions in anitimelanogenesis and antioxidation. Recently, several plants such as Paeonia suf fruticosa and chestnut flower extract have also been reported to show antioxidant and antimelanogenic properties similar to those of Lycium chinense Miller root SFE. The results suggest that Lycium chinense Miller root SFE decreased melanin production due to its depletion of cellular ROS.

Our results indicate that Lycium chinense Miller root SFE inhibited melanogenesis in B16F10 cells by down regulation of both mitogen activated protein kinases and protein kinase A signaling pathways or through its antioxidant properties. Hence, Lycium chinense Miller root SFE could be used as an effective skin anti hyperpigmentation agent. Conclusions This is the first report on the inhibitory effect of Lycium chinense Miller root SFE on melanin synthesis. We also analyzed the antioxidant capacities of the root SFE of Lycium chinense Miller. The present study concluded that Lycium chinense Miller root SFE inhibits melanin synthesis in B16F10 melanoma cells and showed antioxi dant potential.

The present results indicate that the Lycium chinense Miller root SFE inhibited melanin synthe sis in B16F10 melanoma cells by down regulation of both mitogen activated protein kinases and protein kinase A signaling pathways or through its intra cellular antioxidant properties. Hence, the SFE of Lycium chinense Miller root could be applied as a type of der matological anti hyperpigmentation agent in skin care products. Background Alteration of gene expression plays an a role in tumouri genesis and progression of cancer. Modulation of gene expression, for example, tumour suppressors or onco genes, are not exclusively due to mutations and can be manipulated through transcriptional regulation Cilengitide mechan isms which include DNA methylation and histone modifi cation. In cancer cells, the balance between histone acetylation and deacetylation catalyzed by histone acetyltransferases and histone deacetylases, respectively, is often disrupted. For example, altered expression and aberrant recruitment of HDACs have been reported in tumours. HDACs catalyze the removal of acetyl groups from histones resulting in chromatin con densation and transcriptional repression. HDAC inhibitors act to reverse this transcriptional silencing of genes, which include tumour suppressors.