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KMID : 0370220120560020080
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Yakhak Hoeji
2012 Volume.56 No. 2 p.80 ~ p.85
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Role of NADPH Oxidase in the Mechanism of Arachidonic Acid-induced Apoptosis in HepG2 Human Hepatoblastoma Cells
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Nam Jyung-Won
Lee Yong-Soo
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Abstract
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Previously, we have reported that arachidonic acid (AA) appears to be involved in the induction of apoptosis in HepG2 human hepatoblastoma cells. In this study we investigated the possible role of the NADPH oxidase, a membranebound enzyme generating reactive oxygen species (ROS), in the mechanism of AA-induced apoptosis in HepG2 cells. Apoptotic cell death induced by AA was significantly suppressed by various inhibitors of the NADPH oxidase, diphenylene iodonium (DPI), apocynin (Apo) and neopterine (NP). In addition, these inhibitors of the NADPH oxidase completely blunted the AA-induced ROS elevation. Next, we investigated the implication of metabolic pathway of AA in these AA actions. Both apoptosis and ROS production induced by AA were not significantly altered by treatment with indomethacin (Indo) or nordihydroguaiaretic acid (NDGA), selective inhibitors of cyclooxygenase (COX) and lipoxygenase (LOX), respectively, suggesting that AA metabolites produced by COX or LOX may not have an essential role in the AA-induced apoptosis and ROS generation. Collectively, these results suggest that the NADPH oxidase may be a key player in the mechanism of AA-induced apoptosis in HepG2 cells. These results further suggest that NADPH oxidase may be a good target for the management of human hepatomas.
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KEYWORD
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apoptosis, arachidonic acid, NADPH oxidase, reactive oxygen species, HepG2 hepatoblastoma cell
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