Dieta cetogênica em modelo experimental de epilepsia do lobo temporal

Abstract

The ketogenica diet (KD) is indicated in the tratament of distinct disorders as the epilepsy. Studies show that KD may cease the spontaneous seizures in approximately 30% of cases. To contribute to the discussion of the use of DC in epilepsy, this dissertation presents two articles. First is a literature review with the objective of providing a critical view, current and systematic data available regarding antiepileptogenic effect of DC in animal models of temporal lobe epilepsy induced by pilocarpine and kainic acid. The extraction of the data was based on methodological, behavioral, electrophysiological, histologic and molecular parameters. Were included 28 articles, 75% of these used the DC before the Status epilepticus (SE) to prevent the seizures during SE. The KD increases latency for the onset of seizures during SE and decreases frequency of chronic crises. The histologic results the effect of KD is consistently observed for decreasing neuronal death in the CA1 and CA3 regions of the hippocampus. Regarding the molecular analysis, the KD has modulating action on the expression of some genes, mainly those related to apoptosis and inflammatory response. It is also noted that these effects are positively correlated with treatment time not less than 4 weeks. Second article refers to experimental study we investigated the effects of KD containing coconut oil in SE induced by Lithium-pilocarpine. In this study, the effect of DC was investigated the behavior of crises during the SE; in neurodegeneration by immunohistochemistry with Fluoro-Jade; astrogliosis via the expression levels of GFAP; and neuroinflamção through TNF-α expression levels. The experimental groups were: PILO, keto + PILO, keto and NAIVE. We observed that animals treated with DC and submitted to the SE (group keto + PILO) showed no significant difference compared with the group receiving a normal diet and underwent SE (PILO group). The DC decreased neuronal death in the hilus of the hippocampus, 24 hours after SE. The DC increased astrogliosis after 24 hours of the SE, but did not induce significant difference inflammation. Additional studies using the same prospects of our work should be performed in order to contribute to understanding the mechanisms of action of DC and increasing evidence of the use of DC in the context of epilepsy.