Abstract
ABSTRACTIn the present study, we have examined the possible neuroprotective effects of resveratrol and oxyresveratrol against kainic-acid (KA)-induced hippocampal neuronal cell death. Either resveratrol or oxyresvertrol was orally administered 30 min prior to intracerebroventricular (i.c.v.) administration with KA (0.05 μg). Oral pretreatment with oxyresveratrol (50 mg/kg) significantly protected KA-induced hippocampal CA3 neuronal cell death. However, the same dose (50 mg/kg) or a higher dose (100 mg/kg) pretreatment with resveratrol did not affect KA-induced hippocampal neuronal cell death. Furthermore, the i.c.v. pretreatment with 30 μg of oxyresveratrol or resveratrol did not show the protective effect against KA-induced hippocampal neuronal cell death. In the immunohistochemical analysis, FoxO3a and pFoxO3a expressions in the hippocampal CA3 region were significantly increased 30 min after KA administration. Oral pretreatment with oxyresveratrol (50 mg/kg) significantly reduced KA-induced Forkhead homeobox type O3a (FoxO3a) and pFoxO3a expression in CA3 region of the hippocampus, suggesting that oxyresveratrol may exert a neuroprotective effect against KA-induced hippocampal neuronal cell death by reducing the levels of FoxO3a and pFoxO3a protein expression in the hippocampal CA3 region. Furthermore, it is suggested that the neuroprotective effect of orally administered oxyresveratrol against KA-induced neurotoxicity might be possibly mediated by some metabolites rather than direct action of oxyresveratrol on the central nervous system.
Highlights
Kainic acid (KA) is a non-degradable analog of glutamate and is 30-fold more potent in neurotoxicity than glutamate
The results of the present study showed that oral pretreatment with oxyresveratrol exerts a neuroprotective effect against KA-induced hippocampal CA3 neuronal cell death
Several lines evidence have demonstrated that resveratrol shows some neuroprotective effects (Wang et al 2004; Liu et al 2016), the result of the present study suggests that orally treated resveratrol is not effective in for KA-induced neurotoxicity
Summary
Kainic acid (KA) is a non-degradable analog of glutamate and is 30-fold more potent in neurotoxicity than glutamate. Neuronal cell death occurred by KA elicits severe status epilepeticus in the pyramidal layer of the hippocampal CA3 region when KA is administered i.c.v (Sperk 1994). It may be because of excessive activation of neurons by excitatory neurotransmitters (e.g. glutamate), which are massively released as a consequence of energy depletion and which result in excitotoxic neuron death (Beal 1992)
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