[Neuroprotective action of valproic acid accompanied of the modification on the expression of Bcl-2 and activated caspase-3 in the brain of rats submitted to ischemia/reperfusion].

Valproic acid, apart from being known as an anti-epileptic drug, has been proposed in the past few years, as a neuroprotective agent. The purpose of this study was to investigate firstly, if valproic acid protects the neurons from the damage produced by oxidative stress induced by ischemia-reperfusion in the brain of healthy rats, under the transitory occlusion of the right middle cerebral artery. Secondly it was studied if this antiepileptic drug induces changes on the expression of Bcl-2 and activated caspase-3 as a possible mechanism of action on apoptosis. The neurological evaluation of the animals that were subject to ischemia-reperfusion and received valproic acid was better than the ones who didn’t receive it. On another subject, the levels of malondialdehyde on the right cerebral hemisphere in the rats treated with valproic acid were below the levels of the control group in the same hemisphere, whereas the amount of carbonylated proteins was reduced by 67% compared to the control group. Besides, it was found by western blot, that in homogenized brain tissue of the animals under ischemia-reperfusion which received valproic acid, there was a rise on the density of the bands corresponding to Bcl-2, and a reduction of activated 3-capase in comparison to the ones who were not treated with the antiepileptic drug. It’s concluded that the treatment with valproic acid prevented the neurological deficit in healthy rats under Ischemia-reperfusion, blocking the effect of free radicals on lipids and proteins of the affected brain cortex, and it is suggested that the same drug intervenes on apoptosis induced during this type of damage, being able to be a therapeutic alternative in the treatment of cerebral ischemia.