![]() The histopathological changes in the hippocampus were studied using hematoxylin and eosin stain and immunohistochemical stain for brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), beclin-1, nuclear factor kappa-B (NF-κB) and Bcl-2-like protein 4 (BAX). Seizure latency was evaluated, the hippocampus tissue level of antioxidant enzymes was assessed. Material and methods Forty adult male rats were divided into four groups: control, pentylenetetrazol (PTZ) group (injected with PTZ 60 mg/kg, s.c.), pregabalin (Pregb)-PTZ group (pretreated with pregabalin daily 30 mg/kg orally for 1 week) and nilotinib (NIL)-PTZ group (pretreated with nilotinib, 25 mg/kg daily for 1 week) prior to PTZ. Aim of the study was to analyse the neuroprotective and antiepileptic effect of nilotinib and explain its mechanism of action. The proved antioxidant and antifibrotic effect of nilotinib favours its use in the management of epileptic seizures. ![]() Recent studies have attributed the neuronal loss to autophagy. Previous studies have explained neuronal cell death on the basis of cell necrosis and apoptosis. ![]() Introduction Neuronal cell death and glial cell activation are the main pathological findings induced by seizures secondary to oxidative stress.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |