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The synergistic effect of 1′‐acetoxychavicol acetate and sodium butyrate on cell death of human hepatocellular carcinoma cells
Author(s) -
Kato Rie,
MatsuiYuasa Isao,
Azuma Hideki,
KojimaYuasa Akiko
Publication year - 2013
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.27.1_supplement.636.6
Subject(s) - sodium butyrate , intracellular , nadph oxidase , reactive oxygen species , chemistry , apoptosis , catalase , programmed cell death , butyrate , cancer cell , cell growth , cell , microbiology and biotechnology , cancer research , biochemistry , oxidative stress , biology , cancer , genetics , fermentation , gene
1′‐Acetoxychavicol acetate (ACA), obtained from alpinia galangal , exhibits chemopreventive effects on chemically induced tumor formation. Sodium butyrate (NaB), one of the major short chain fatty acids, is known to inhibit cancer cell proliferation in tumor cells. The interaction between ACA and NaB is still unclear. Here, we examined the effect of ACA and NaB on cell death of HepG2 cells. Methods The cell number was measured by neutral red assay. Intercellular reactive oxygen species (ROS) was measured by DCFH‐DA assay. Results The cell number of HepG2 cells was synergistically decreased with the combined treatment of ACA and NaB, resulting from apoptotic cell death. In ACA and NaB simultaneously treated cells, intercellular ROS also increased significantly. However, the cell number in ACA and NaB treated cells was improved with the treatment of catalase. The increase in intercellular ROS was prevented with DPI, the inhibitor of NADPH oxidase. These events weren't observed in normal cells. Conclusion ACA and NaB synergistically induce apoptotic cell death via the activation of NADPH oxidase and the increase in the intercellular ROS, and the effect is specific to carcinoma cells.