Original Articles
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jun 21, 2009; 15(23): 2870-2877
Published online Jun 21, 2009. doi: 10.3748/wjg.15.2870
Alisol B acetate induces apoptosis of SGC7901 cells via mitochondrial and phosphatidylinositol 3-kinases/Akt signaling pathways
Yong-Hong Xu, Li-Jie Zhao, Yan Li
Yong-Hong Xu, Li-Jie Zhao, Yan Li, Department of Digestive Diseases, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China
Author contributions: Xu YH and Li Y contributed equally to this work; Xu YH and Li Y designed the research; Xu YH performed the research; Xu YH and Zhao LJ analyzed data; Xu YH wrote the paper; Li Y helped organize, wrote and corrected the paper.
Correspondence to: Yan Li, Professor, Department of Digestive Diseases, Shengjing Hospital, China Medical University, Shenyang 110004, Liaoning Province, China. yanli0227@126.com
Telephone: +86-24-83956416
Fax: +86-24-23582697
Received: March 13, 2009
Revised: May 7, 2009
Accepted: May 14, 2009
Published online: June 21, 2009
Abstract

AIM: To examine the effect of alisol B acetate on the growth of human gastric cancer cell line SGC7901 and its possible mechanism of action.

METHODS: The cytotoxic effect of alisol B acetate on SGC7901 cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Phase-contrast and electron microscopy were used to observe the morphological changes. Cell cycle and mitochondrial transmembrane potential (Δψm) were determined by flow cytometry. Western blotting was used to detect the expression of apoptosis-regulated gene Bcl-2, Bax, Apaf-1, caspase-3, caspase-9, Akt, P-Akt and phosphatidylinositol 3-kinases (PI3K).

RESULTS: Alisol B acetate inhibited the proliferation of SGC7901 cell line in a time- and dose-dependent manner. PI staining showed that alisol B acetate can change the cell cycle distribution of SGC7901, increase the proportion of cells in G0-G1 phase and decrease the proportion of S phase cells and G2-M phase cells. Alisol B acetate at a concentration of 30 &mgr;mol/L induced apoptosis after 24, 48 and 72 h incubation, with occurrence rates of apoptotic cells of 4.36%, 14.42% and 21.16%, respectively. Phase-contrast and electron microscopy revealed that the nuclear fragmentation and chromosomal condensed, cells shrank and attachment loss appeared in the SGC7901 treated with alisol B acetate. Apoptosis of SGC7901 cells was associated with cell cycle arrest, caspase-3 and caspase-9 activation, loss of mitochondrial membrane potential and up-regulation of the ratio of Bax/Bcl-2 and inhibition of the PI3K/Akt.

CONCLUSION: Alisol B acetate exhibits an anti-proliferative effect in SGC7901 cells by inducing apoptosis. Apoptosis of SGC7901 cells involves mitochondria-caspase and PI3K/Akt dependent pathways.

Keywords: Alisol B acetate; Apoptosis; Mitochondria; Phosphatidylinositol 3-kinases/Akt; SGC7901 cells