This study was conducted to investigate the effect of branch extracts of Vaccinium oldhamii (VOB) on melanin synthesis in B16F10 cells. VOB promoted melanin production in absence or presence of α-melanocyte-stimulating hormone (α-MSH) in B16F10 cells. However, VOB did not affect the expression of tyrosinase and TRP-1 associated with melanin synthesis at the mRNA and protein levels in B16F10. But, VOB decreased TRP-2 protein level and induced tyrosinase activation in B16F10 cells. Inhibition of tyrosinase activity and tyrosinase knockdown attenuated VOB-mediated melanin synthesis. In conclusion, VOB may stimulate melanin synthesis through activating tyrosinase activity.

In this study, we investigated the effect of the extracts from Vaccinium oldhamii on cell proliferation and the regulatory mechanisms of cyclin D1 protein level in human cancer cells. The branch extracts from Vaccinium oldhamii (VOB) showed higher inhibitor effect against the cell growth than leave extracts (VOL) and fruit extracts (VOF) in human colorectal cancer, breast cancer, prostate cancer, non-small lung cancer, pancreatic cancer and liver cancer cells. In addition, VOB decreased cyclin D1 level at both protein and mRNA level. MG132 treatment attenuated VOB-mediated cyclin D1 downregulation. A point mutation of threonine-286 to alanine attenuated cyclin D1 degradation by VOB. In addition, the inhibition of nuclear export by leptomycin B (LMB) attenuated cyclin D1 degradation by VOB. But, the treatment of PD98059 (ERK1/2 inhibitor), SB203580 (p38 inhibitor), SP600125 (JNK inhibitor), LiCl (GSK3β inhibitor), LY294002 (PI3K inhibitor) or BAY 11-7082 (IκK inhibitor) did not affect VOB-induced cyclin D1 degradation. In conclusion, VOB induced cyclin D1 degradation through redistribution of cyclin D1 from the nucleus to cytoplasm via T286 phosphorylation of cyclin D1, which resulted in the inhibition of cancer cell proliferation.