The synergistic antiproliferative effect of pterostilbene and acetylshikonin on B16 F10 cells
10.3969/j.issn.1001-1978.2016.06.016
- VernacularTitle:紫檀茋和乙酰紫草素抑制B16 F10细胞增殖的协同作用
- Author:
Hong CHEN
;
Shanshan ZHANG
;
Jinlei DONG
;
Jing ZHONG
;
Xiaoqin WANG
;
Bo ZHANG
- Publication Type:Journal Article
- Keywords:
melanoma;
pterostilbene;
acetylshikonin;
drug combination;
apoptosis;
cell cycle;
tumor inhibi-tion rate
- From:
Chinese Pharmacological Bulletin
2016;32(6):818-824
- CountryChina
- Language:Chinese
-
Abstract:
Aim Toevaluatethesynergisticeffectof anti-tumor by the pterostilbene and acetylshikonin act-ing on B16F10 cells and investigate the interrelated mechanisms.Methods Theresearchscreenedandan-alyzed the target-related of pterostilbene and ace-tylshikonin by system-pharmacological methods. The proliferative inhibition rate of B16F10 cells were meas-ured by MTT.The apoptosis in B16F10 cells were proved by both cellular morphological and biochemical methods.The expression of apoptotic genes were as-sessed via RT-PCR.The apoptotic rate and cell cycle were measured by flow cytometry.Melanoma models were established in C57BL/6 mice,and the inhibitory rateoftumorgrowthwasmeasured.Results The14 targets of pterostilbene were closely related to cell cy-cle,acetylshikonin′s 12 targets displayed a relationship with apoptosis,and correlated with p53 signaling path-way.Pterostilbene along with acetylshikonin signifi-cantly inhibited cell proliferation of B16F10 cells in a dose-dependent way and resulted a remarkable syner-gistic effect.The apoptotic rate reached highest with a blocked-cell cycle at G1 phase in the co-treatment group.The RT-PCR results showed that the expres-sions of p53,Bax and p21 were up-regulated and the expressions of Bcl-2,CDK2 and Cyclin E were down-regulated with time.The changes of p53,Bax and Bcl-2 were obvious in combined treated group.All treat-ments in vivo showed different tumor inhibition rates while co-treatment group showed highest.Conclusion Pterostilbenecooperatedwithacetylshikonininhibits the proliferation in B16F10 cells,and activates the p53 signaling pathway to induce the B16F10 cells apoptosis and a cell cycle arrest.
