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The synergistic effect of 1’‐acetoxychavicol acetate and sodium butyrate on the death of human hepatocellular carcinoma cells (644.17)
Author(s) -
MatsuiYuasa Isao,
Kato Rie,
Azuma Hideki,
KojimaYuasa Akiko
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.644.17
Subject(s) - ampk , intracellular , sodium butyrate , chemistry , catalase , nadph oxidase , butyrate , apoptosis , reactive oxygen species , protein kinase a , amp activated protein kinase , cancer cell , programmed cell death , microbiology and biotechnology , cell growth , phosphorylation , cancer research , biochemistry , oxidative stress , cancer , biology , medicine , fermentation , gene
It has been suggested that the combined effect of natural products may improve the effect of treatment against the proliferation of cancer cells. We evaluated the combination of 1’‐acetoxychavicol acetate (ACA), obtained from Alpinia galangal, and sodium butyrate (NaB), a major short chain fatty acid, on the growth of HepG2 cells and found that treatment had a synergistic inhibitory effect. The number of HepG2 cells was synergistically decreased via apoptosis induction with the combined treatment of ACA and NaB. In ACA‐ and NaB‐treated cells, intracellular reactive oxygen species (ROS) levels and NADPH oxidase activities were increased significantly. The decrease in cell number after combined treatment of ACA and NaB was improved with the treatment of catalase. These results suggest that an increase in intracellular ROS levels is involved in cancer cell death. AMP‐activated protein kinase (AMPK) plays an essential role in controlling processes related to tumor development. In ACA‐ and NaB‐treated cells, AMPK phosphorylation was induced significantly, and this induction improved when cells were pretreated with catalase. These results suggest that the increase in intracellular ROS is involved in the increase of AMPK phosphorylation. In conclusion, combined treatment with ACA and NaB synergistically induced apoptotic cell death via an increase in intracellular ROS and phosphorylation of AMPK.