hepatocyte growth factor attenuates the severity of status epilepticus in kainic acid-induced model of temporal lobe epilepsy by targeting apoptosis and astrogliosis

Introduction: although pharmacotherapy is the most common treatment for epilepsy, properseizure control is not achieved with current medications. this study evaluated the protectiveeffects of the hepatocyte growth factor (hgf) in a rat model of temporal lobe epilepsy(tle) and explored possible molecular mechanisms.methods: a tle rat model was determined using an intra-hippocampal kainic acid injection(4 μg). intra-cerebrovascular injection of hgf (6 μg) was performed 30 min before kainicacid injection. learning and memory impairment were investigated by behavioral tests. theenzyme-linked immunosorbent (elisa) was used to determine astrogliosis and dnafragmentation. changes in neuronal density and mossy fiber sprouting were evaluated by nissland timm staining, respectively.results: behavioral assessments indicated that kainate-treated rats presented spontaneousseizures. moreover, their alternation percentage scores in the y-maze test were lower(p<0.001). likewise, the passive avoidance test confirmed learning disability in kainate-treatedrats (p<0.001). hgf administration reduced the number of spontaneous seizures, alternationpercentage score (p<0.001), and cognitive disturbances (p<0.001). the histopathologicalresults also showed that a protected hgf administration contributed to the reduction ofneuronal loss in the ca3 subregion of the hippocampus and inhibited the formation of aberrantmossy fiber sprouting (mfs) (p<0.01). furthermore, the elisa data indicated a significantdecrease in gfap (p<0.01) and dna fragmentation (p<0.05) following hgf administration.conclusion: our findings demonstrated the validity of hgf in protection against theprogression of the kainate-induced tle in rats. this measure improved learning, cognitivedisturbances and inhibited apoptosis and astrogliosis.