Curcumin combined FOLFOX induced cell apoptosis of gastric cancer and its mechanism research.
- Author:
Xiang ZHOU
1
;
Tao YOU
;
Wei-Ming WANG
;
Zhi-Qiang ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Combined Chemotherapy Protocols; pharmacology; Apoptosis; drug effects; Caspase 3; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Curcumin; pharmacology; Fluorouracil; pharmacology; Humans; Leucovorin; pharmacology; Organoplatinum Compounds; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Stomach Neoplasms; pathology; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2013;33(6):810-813
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of curcumin combined folinic acid fluorouracil oxaliplatin (FOLFOX) on the gastric adenocarcinoma cell line BGC-823 and to explore its possible mechanisms.
METHODSCells were divided into five groups, i.e. the blank control group, the curcumin group, the FOLFOX group (0.1 mmol/L 5-FU +5 micromol/L oxaliplatin), and the curcumin combined FOLFOX group. CCK-8 was used to detect cell activity. The cell apoptosis was observed using Hoechst dyeing. Caspase-3 test kit was applied to test Caspase-3 vitality. The mRNA expressions of Bcl-2 and Bax were detected by real time fluorescent quantitative PCR. The expressions of Bcl-2 and Bax protein were determined by Western blot.
RESULTSThe BGC-823 cells' proliferation could be inhibited, apoptosis induced, the Caspase-3 activity increased, expressions of Bcl-2 mRNA and Bcl-2 protein lowered, while Bax mRNA and Bax protein expressions increased in each medicated group. Besides, the efficacy of the curcumin combined FOLFOX group was superior to that of the curcumin group and the FOLFOX group, showing statistical difference (P < 0.01).
CONCLUSIONCurcumin combined FOLFOX could significantly inhibit the proliferation of BGC-823 cells possibly via promoting Bax expression and Caspase-3 activity, inhibiting Bcl-2 expression, thus inducing apoptosis.