licochalcone-a and Seizures

The mitogen-activated protein kinase family (MAPK) is an important group of enzymes involved in cellular responses to diverse external stimuli. One of the members of this family is the c-Jun-N-terminal kinase (JNK). The activation of the JNK pathway has been largely associated with the pathogenesis that occurs in epilepsy and neurodegeneration. Kainic acid (KA) administration in rodents is an experimental approach that induces status epilepticus (SE) and replicates many of the phenomenological features of human temporal lobe epilepsy (TLE). Recent studies in our group have evidenced that the absence of the JNK1 gene has neuroprotective effects against the damage induced by KA, as it occurs with the absence of JNK3. The aim of the present study was to analyse whether the pharmacological inhibition of JNK1 by Licochalcone A (Lic-A) had similar effects and if it may be considered as a new molecule for the treatment of SE. In order to achieve this objective, animals were pre-treated with Lic-A and posteriorly administered with KA as a model for TLE. In addition, a comparative study with KA was performed between wild type pre-treated with Lic-A and single knock-out transgenic mice for the Jnk1

Topics: Animals; Anticonvulsants; Cell Survival; Chalcones; Hippocampus; Inflammation; Kainic Acid; Mice, Inbred C57BL; Mice, Knockout; Mitogen-Activated Protein Kinase 8; Neurons; Neuroprotection; Neuroprotective Agents; Oxidative Stress; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-bcl-2; Seizures