@article{oai:nagasaki-u.repo.nii.ac.jp:00016461,
 author = {Shibata, Hidetaka and Ichikawa, Tatsuki and Nakao, Kazuhiko and Miyaaki, Hisamitsu and Takeshita, Shigeyuki and Akiyama, Motohisa and Fujimoto, Masumi and Miuma, Satoshi and Kanda, Shougo and Yamasaki, Hironori and Eguchi, Katsumi},
 issue = {3},
 journal = {Molecular Medicine Reports},
 month = {May},
 note = {Oxidative stress is known to play a key role in the progression of liver disease, including non-alcoholic steatohepatitis (NASH), which is often accompanied by hyperglycemia. This study examined the influence of high glucose on oxidative stress-induced hepatic cell death. Hc cells, a normal human hepatocyte-derived cell line, were cultured in normal-to-high glucose (5.5-22 mM)-containing medium with varying concentrations (0.01-1 mM) of hydrogen peroxide. In certain experiments, cyclosporine A (CyA), which inhibits the mitochondrial permeability transition (MPT) pore, or Z-VAD-FMK (z-VAD), a pan-caspase inhibitor, were added to the medium. Cell viability was evaluated using a colorimetric assay. The mode of cell death was determined by nuclear staining methods using Hoechst 33258 and Sytox green. Neither high glucose (22 mM) nor 0.05-0.5 mM of hydrogen peroxide alone killed Hc cells. However, a combination of the two induced cell death, causing the nuclei of Hc cells to become expanded rather than condensed, and the nuclear membrane to become weak. CyA, but not z-VAD, blocked cell death. These results suggest that a high glucose condition may cause human hepatocytes to undergo hydrogen peroxide-induced necrotic cell death., Molecular Medicine Reports, 1(3), pp.379-385; 2008},
 pages = {379--385},
 title = {A high glucose condition sensitizes human hepatocytes to hydrogen peroxide-induced cell death},
 volume = {1},
 year = {2008}
}