Allicin induces apoptosis of the MGC-803 human gastric carcinoma cell line through the p38 mitogen-activated protein kinase/caspase-3 signaling pathway

作者：Zhang, Xuecheng^*; Zhu, Yong; Duan, Wei; Feng, Chen; He, Xuan

来源：Molecular Medicine Reports, 2015, 11(4): 2755-2760.

DOI：10.3892/mmr.2014.3109

• p38 mitogen-activated protein kinase
• caspase-3
• allicin
• gastric carcinoma
• apoptosis

Gastric cancer is one of the most common forms of malignant tumor, and the development of anti-gastric cancer drugs with minimal toxicity is of clinical importance. Allicin is extracted from Allium sativum (garlic). Recent research, including clinical experiments, has shown that garlic has anticancer and tumor suppressive effects. The present study aimed to investigate the effects of allicin on the MGC-803 human gastric carcinoma cell line, and to further explore the possible mechanisms of its tumor suppressor effects. The effects of allicin on the MGC-803 cells were initially examined using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst staining was also used, in order to demonstrate the impact of allicin on MGC-803 cell apoptosis. In addition, western blot analysis was performed to determine the abnormal expression levels of apoptosis-associated proteins, following the treatment of MGC-803 cells with allicin. Western blotting was also used to investigate the specific mechanisms underlying allicin-induced apoptosis of MGC-803 cells. The rate of MGC-803 apoptosis was significantly increased, when the concentration and treatment time of allicin were increased. Hoechst staining detected an enhanced rate of apoptosis, and enhanced expression levels of cleaved caspase 3 were determined by western blotting. Notably, the protein expression levels of p38 were increased when the MGC-803 cells were treated with allicin. The results of the present study suggest that allicin may inhibit the proliferation and induce the apoptosis of MGC-803 human gastric carcinoma cells, and this may partially be achieved through the enhanced expression of p38 and cleaved caspase 3.

• 出版日期2015-4