Abstract
One of the pathways by which alcohol induces hepatocyte apoptosis is via oxidative stress. We screened several chemically-synthesized small molecules and found LAS-0811, which inhibits oxidative stress. In this study, we elucidated its role in inhibiting alcohol-induced apoptosis in hepatocyte-like VL-17A cells. VL-17A cells were pre-incubated with LAS-0811, followed by ethanol incubation. Ethanol-induced reactive oxygen species and apoptosis were significantly inhibited in LAS-0811 pre-treated cells. VL-17A cells were transfected with a reporter (ARE/TK-GFP) plasmid containing green fluorescent protein (GFP) as a reporter gene and the anti-oxidant response element as the promoter. LAS-0811 pre-treatment significantly induced the GFP expression compared to the cells treated with ethanol alone. LAS-0811 induced the activation of nrf2 and enhanced the expression and activity of glutathione peroxidase, one of the downstream targets of nrf2. The results indicate that LAS-0811 protects VL-17A cells against ethanol-induced oxidative stress and apoptosis at least in part via nrf2 activation.
Original language | English |
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Pages (from-to) | 876-881 |
Number of pages | 6 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 379 |
Issue number | 4 |
DOIs | |
State | Published - 20 Feb 2009 |
Bibliographical note
Funding Information:We thank the GlaxoSmithKline Research Fund of the Korean Association for the Study of the Liver for supporting Tae-Hun Kim.
Keywords
- Alcohol
- Liver
- Nrf2
- Oxidative stress
- Small molecule