Gastric Cancer
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jul 28, 2007; 13(28): 3824-3828
Published online Jul 28, 2007. doi: 10.3748/wjg.v13.i28.3824
Induction of apoptosis of human gastric carcinoma SGC-7901 cell line by 5, 7-dihydroxy-8-nitrochrysin in vitro
Xiao-Hong Ai, Xing Zheng, Xiao-Qing Tang, Li Sun, Yang-Qin Zhang, Yong Qin, Hua-Qing Liu, Hong Xia, Jian-Guo Cao
Xiao-Hong Ai, Department of Oncology, First Affiliated Hospital, Nahua University, Hengyang 421001, Hunan Province, China
Xiao-Hong Ai, Xiao-Qing Tang, Li Sun, Yang-Qin Zhang, Yong Qin, Hua-Qing Liu, Hong Xia, Jian-Guo Cao, Institute of Oncology, Nahua University, Hengyang 421001, Hunan Province, China
Xing Zheng, Xiao-Qing Tang, Li Sun, Yang-Qin Zhang, Yong Qin, Hua-Qing Liu, Hong Xia, Jian-Guo Cao, Institute of Pharmacology, Nahua University, Hengyang 421001, Hunan Province, China
Xiao-Qing Tang, School of Pharmaceutical Science, Central South University, Changsha 410078, Hunan Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Jian-Guo Cao, Institute of Pharmacology, Nahua University, Hengyang 421001, Hunan Province, China. caojianguo2005@yahoo.com.cn
Telephone: +86-734-8281510 Fax: +86-734-8281305
Received: March 26, 2007
Revised: April 13, 2007
Accepted: April 18, 2007
Published online: July 28, 2007
Abstract

AIM: To investigate the effect of 5, 7-dihydroxy-8-nitrochrysin (NOChR) on apoptosis of human gastric carcinoma SGC-7901 cell line.

METHODS: SGC-7901 cells were cultured in vitro and the inhibitory effect of NOChR on proliferation of SGC-7901 cells was measured by using an MTT assay. NOChR-induced apoptosis rate of SGC-7901 cells was detected using flow cytometry (FCM) with PI staining. DNA ladder bands were observed by DNA agarose gel electrophoresis. The influence of NOChR on the proxisome proliferator-activated receptor-γ (PPARγ), Bcl-2 and Bax protein expression of SGC-7901 cells was analyzed by Western blot.

RESULTS: MTT assay showed that NOChR markedly inhibited proliferation of SGC-7901 cells in a dose-dependent manner, and when IC50 was 4.14 μmol/L, the potency of NOChR was 10 times than that of lead compound, chrysin (ChR, IC50 was 40.56 μmol/L), and was similar to 5-fluorouracil (5-FU, IC50 was 4.51 μmol/L). FCM with propidium iodide (PI) staining demonstrated that the apoptosis rates of SGC-7901 cells treated with 1.25, 5.00 and 20.00 μmol/L NOChR for 48 h were 9.8% ± 0.2%, 36.8% ± 1.9% and 45.5% ± 3.5%, respectively, and were significantly higher when treated with 5.00 and 20.00 μmol/L NOChR than that with 20.00 μmol/L ChR (12.9% ± 1.5%). DNA agarose gel electrophoresis showed that treatment of SGC-7901 cells with 20.00 μmol/L NOChR for 48 h resulted in typical DNA ladder bands of DNA of SGC-7901 cells, which could be eliminated by treating with 10.00 μmol/L GW9662, a blocker of PPARγ. Western blot analysis revealed that after 24 h of treatment with 20.00 μmol/L NOChR, PPARgamma and Bax protein expression of SGC-7901 cells increased but Bcl-2 expression decreased; however, pre-incubation with 10.00 μmol/L GW9662 could efficiently antagonize and weaken the regulatory effect of 20.00 μmol/L NOChR on Bax and Bcl-2 protein expression of SGC-7901 cells.

CONCLUSION: NOChR induces apoptosis of SGC-7901 cell lines by activating PPARγ and decreasing ratio of Bcl-2 to Bax.

Keywords: Gastric neoplasm, Chrysin, Chrysin derivatives, Apoptosis, Proxisome proliferator-activated receptorγ, Bcl-2, Bax