Inhibitory effects of Licochalcone A on proliferation of melanoma B16 F10 cells
10.3969/j.issn.1001-1978.2015.07.016
- VernacularTitle:甘草查尔酮A抑制小鼠黑色素瘤B16 F10细胞增殖机制研究
- Author:
Yanming WANG
;
Ying LIU
;
Xinyan YAN
;
Lingling SI
;
Caixia GAO
;
Lina YU
;
Qiusheng ZHENG
- Publication Type:Journal Article
- Keywords:
B16 F10;
Licochalcone A;
the rate of proliferation;
melanin level;
differentiation;
apoptosis;
cell cycle arrest
- From:
Chinese Pharmacological Bulletin
2015;(7):967-972
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the mechanism of the melanoma B16 F10 cells proliferation induced by Lico-chalcone A in vitro. Methods The proliferation of B16 F10 cells induced by Licochalcone A was deter-mined by SRB method. The morphological changes were observed using Giemsa staining under the phase contrast microscope equipped with a digital camera. The melanin level was assessed by colorimetric meth-od. The apoptotic rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. The mRNA expression levels of B cell lymphoma/lewkmia-2 ( Bcl-2 ) , Bcl-2 associated X protein ( Bax) , the cell cycle protein CyclinE2 and cyclin-dependent kinase-2 ( CDK2 ) CDK2 were detec-ted using Q-PCR analysis. Results The proliferation of B16 F10 cells treated with Licochalcone A was effec-tively inhibited in a concentration and time-dependent manner. A clear morphological change was observed with the increasing concentration of Licochalcone A in B16F10 cells, the dendrite-like projections changed to the narrowing ball shape, which was associated with the increasing melanin level. The low concentration of Licochalcone A could induce B16F10 differentiation, and the high concentration of Licochalcone A could in-duce B16F10 apoptosis, which was accompanied with the increasing G1 phase in cell cycle. The mRNA ex-pression levels of Bcl-2 /Bax, CyclinE2 and CDK2 were markedly reduced. Conclusion Licochalcone A can effectively inhibit the proliferation of B16 F10 cells, induced cell cycle arrest at G1 phase, and fur-ther induced differentiation and apoptosis.
