Abstract
We aimed to reveal the anti-convulsant effects sulfasalazine and its mechanism in pentylenetetrazole (PTZ)-induced seizures in rats. Forty-eight male Wistar albino rats (200-250 g) were randomly divided into two groups: 24 for electroencephalography (EEG) recording (group A) and 24 for behavioral studies (group B). About 70 mg/kg PTZ was used for behavioral studies after sulfasalazine administration and 35 mg/kg PTZ was used for EEG recording after sulfasalazine administration. Electrodes were implanted on the dura mater over the left frontal cortex and the reference electrode was implanted over the cerebellum for EEG recording. Racine’s convulsion scale, first myoclonic jerk onset time, spike percentages, brain malondialdehyde (MDA), superoxide dismutase (SOD), and prostaglandin F2α (PGF2α) levels were evaluated between the groups. First myoclonic jerk onset time was significantly shorter in the saline group than both 250 and 500 mg/kg sulfasalazine groups (P<0.05). Racine's convulsion scores were significantly lower in the 250 and 500 mg/kg sulfasalazine groups than the saline group (P<0.05, P<0.001). The two sulfasalazine groups had lower spike percentages than the saline group (P<0.05). Significantly lower MDA and PGF2α levels were observed in the 250 and 500 mg/kg sulfasalazine groups compared with the saline group (P<0.05, P<0.001, respectively). SOD increased significantly in both sulfasalazine groups compared with the PTZ+saline group (P<0.05). Our study demonstrated that sulfasalazine had protective effects on PTZ-induced convulsions by protecting against oxidative and inflammatory damage associated with PTZ.
Highlights
Neuroinflammation is a complex process that involves the activation of microglia, astrocytes, and endothelial cells in the blood-brain barrier, the infiltration of plasma proteins and immune system cells into the brain tissue, and the interaction of inflammation-related mediators with the brain tissue [1]
Neuroinflammation signs are found in many central nervous system diseases, and epilepsy is often associated with neuroinflammation
Recurrent seizures are observed in autoimmune diseases accompanied by severe and prolonged neuroinflammation and in encephalitis patients, and neuroinflammation is frequently observed in epilepsies resistant to anticonvulsant drugs [3]
Summary
Neuroinflammation is a complex process that involves the activation of microglia, astrocytes, and endothelial cells in the blood-brain barrier, the infiltration of plasma proteins and immune system cells into the brain tissue, and the interaction of inflammation-related mediators with the brain tissue [1]. The first concerns drugs like lorazepam and other benzodiazepines that reduce symptomatic seizures by increasing gaba-aminobutyric acid receptor-A (GABA-AR) mediated inhibition, and the second concerns drugs that contain phenytoin and carbamazepines, which are responsible for activating voltage-gated Na+ channels and have the effect of decreasing the potential [5,6,7,8]. Their use is limited in many patients due to their strong and intolerable side effects [9]. These treatments are symptomatic and do not contribute to the basic pathological processes and diseases associated with epilepsy [10]
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