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Rutin upregulates neurotrophic factors resulting in attenuation of ethanol-induced oxidative stress in HT22 hippocampal neuronal cells.

BACKGROUND
Alcoholism, which refers to the excessive consumption of alcohol, has deleterious effects on personal and social health worldwide. Oxidative stress evoked by ethanol plays an important role in the pathogenesis of neurodegenerative diseases. Rutin is a bioflavonoid that has been demonstrated to scavenge superoxide radicals. However, the effects of rutin on neuronal toxicity following ethanol-induced oxidative stress have not previously been investigated. Thus we investigated the antioxidant effect of rutin in hippocampal neuronal cells (HT22 cells) exposed to ethanol.


RESULTS
We found that rutin pretreatment prevented the ethanol-induced decrease in protein level expression of nerve growth factor, glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) in HT22 cells. Cell viability as analyzed by the MTT method revealed a significant increase in cell viability in the rutin-treated group compared with the ethanol-only treated group. Antioxidant effect of rutin was confirmed to be due to reduction of intracellular reactive oxidative species production in ethanol-treated HT22 cells. Moreover, rutin significantly increased the level of the antioxidant glutathione, and the activities of the antioxidant enzymes superoxide dismutase and catalase.


CONCLUSION
These findings indicate that rutin has potential as a therapeutic agent to treat alcohol-related neurodegenerative disorders.