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- W2000504699 abstract "Apomorphine, therapeutically used for Parkinson's disease, is a dopamine D1/D2 receptor agonist that has been determined to be a potent antioxidant and to prevent the reaction of free radicals in the brain. Alcohol is a neurotoxic agent that induces neurodegeneration possibly through the generation of free radicals. In this study, we investigated the antioxidant potential of apomorphine upon ethanol-induced neurodegeneration in the cortex of adult rats. Ethanol-induced apoptotic neurodegeneration was measured via the suppression of Bcl-2, the induction of Bax, the release of cytochrome C and the activation of caspase-9 and caspase-3. Moreover, ethanol-induced elevated levels of cleaved PARP-1 indicated exaggerated neuronal DNA damage. Our results demonstrated the neuroprotective effect of apomorphine by reversing the ethanol-induced apoptotic trend as observed by the increased expression of Bcl-2, down regulation of Bax, inhibition of mitochondrial cytochrome C release and inhibition of activated caspase-9 and caspase-3. Moreover, apomorphine treatment further decreased the expression of cleaved PARP-1 to reveal a reduction in ethanol-induced neuronal damage. Immunohistochemical analysis and Nissl staining also revealed neuroprotective effect of apomorphine after ethanol-induced neuronal cell death. In this study, our results indicated that apomorphine at doses of 1 and 5mg/kg has neuroprotective effects for ethanol-induced neuronal damage. Finally, we can conclude that apomorphine has effective therapeutic potential to protect the brain against ethanol-induced neurotoxicity." @default.
- W2000504699 created "2016-06-24" @default.
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- W2000504699 date "2014-07-01" @default.
- W2000504699 modified "2023-10-16" @default.
- W2000504699 title "Apomorphine attenuates ethanol-induced neurodegeneration in the adult rat cortex" @default.
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- W2000504699 doi "https://doi.org/10.1016/j.neuint.2014.04.009" @default.
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