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It was ground to form a white to yellowish powder and dissolved in 0.5% (CMC) and given to rats according to the determined dose.įorty male adult rats (200 to 250 gm body weight) were obtained from the animal house of the Urology and Nephrology Centre, Manasoura University. Nilotinib was purchased from (TASIGNA® 200 mg capsule, Novartis Pharmaceuticals UK Ltd Dublin, Ireland). Pentylenetetrazol (PTZ) (P6500, Millipore-Sigma, St Louis, MO, USA) was dissolved in 0.9% sterile normal saline. Pregabalin (LYRICA CR®-pregabalin tablet, 0071-1027, Pfizer Inc., Giza, Egypt) was suspended in 0.5% carboxymethyl cellulose (CMC). The possible neuroprotective effect of NIL as a new antiepileptic drug on experimentally-induced acute epilepsy in rats was the aim of this study. However, studies investigating this effect on experimental models of epilepsy are limited. The antioxidant and antifibrotic effects of NIL favour its use in the management of epileptic seizures. In Alzheimer’s disease, it was found that NIL reduced amyloid accumulation and autophagic activities which was explained by tyrosine kinase inhibition and restoration of parkin-beclin-1 interaction.
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Some studies proved that NIL has a favourable action in reducing oxidative stress and fibrosis in the rat model for renal disorders and liver injuries. Nilotinib (NIL) has been identified as a recent phenyl amino-pyrimidine derivative with marked selectivity against the Bcr-Abl tyrosine kinase. Resistance to anti-epileptics was reported in one-third of epileptic patients according to Pulman et al. Although Pregb is well tolerated, many side effects have been reported including the two most common, dizziness and sedation, along with peripheral oedema, dry mouth, and teratogenicity. Pregb acts by inhibiting release of glutamate from the presynaptic neurons by interaction with glial fibrillary acidic protein (GFAP) receptors. Pregabalin (Pregb, Lyrica®, Pfizer) is a routinely used antiepileptic with acceptable safety and tolerability and was approved as a monotherapy for the management of refractory epilepsy. Antiepileptic drugs having antioxidant properties were proven to have a neuroprotective effect on animals. Epileptic seizures are always associated with the formation of reactive oxygen species (ROS) and oxidative stress in animal models of epilepsy. However, the detailed mechanism of autophagy accompanying epilepsy is still unclear.
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Many studies proved that modifying autophagy can mitigate the outcome of an epileptic seizure.
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Unfortunately, autophagy can paradoxically progress to cell death with prolonged stress. Simply it is the process by which cells break down and reuse their organelles and macronutrients to maintain survival. Īutophagy occurs in all eukaryotic cells as an important process for the maintenance of the intracellular homeostasis. Recent studies attributed the neuronal loss to a type of programmed cell death, called autophagy. Previous studies on epilepsy pathogenesis explained neuronal cell death which occurs in epileptic seizures and was based on cell necrosis and apoptosis. Prevention of neuron loss and the glial cell activation has been a major aim of pharmaceutical research. The neurons of the hippocampus and the hilus of the dentate gyrus were the most affected brain areas. Previous studies reported the main pathological findings following epileptic seizures were neuronal cell death and glial cell activation. Epileptic seizures trigger neuronal death by a variety of mechanisms, of which, oxidative stress is the most common cause. Epilepsy is a common chronic neurological disorder characterized by spontaneous recurrent seizures, affecting millions of people of all ages all over the world.