Department of Emergency Medicine, Izmir Katip Çelebi University Atatürk Training and Research Hospital, Izmir, Turkey.
Department of Physiology, Demiroğlu Bilim University Faculty of Medicine, Istanbul, Turkey.
Braz J Med Biol Res. 2021 Dec 3;54(12):e11541. doi: 10.1590/1414-431X2021e11541. eCollection 2021.
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.
我们旨在揭示柳氮磺胺吡啶（Sulfasalazine）在戊四氮（PTZ）诱导的大鼠癫痫发作中的抗惊厥作用及其机制。将 48 只雄性 Wistar 白化大鼠（200-250g）随机分为两组：24 只为脑电图（EEG）记录组（A 组），24 只为行为研究组（B 组）。Sulfasalazine 给药后，用约 70mg/kgPTZ 进行行为研究，Sulfasalazine 给药后用 35mg/kgPTZ 进行 EEG 记录。将电极植入左侧额皮质硬脑膜上，参考电极植入小脑进行 EEG 记录。评估各组之间的 Racine 惊厥评分、首次肌阵挛发作起始时间、棘波百分比、脑丙二醛（MDA）、超氧化物歧化酶（SOD）和前列腺素 F2α（PGF2α）水平。与生理盐水组相比，Sulfasalazine 组的首次肌阵挛发作起始时间显著缩短（P<0.05）。与生理盐水组相比，Sulfasalazine 组的 Racine 惊厥评分明显降低（P<0.05，P<0.001）。Sulfasalazine 组的棘波百分比低于生理盐水组（P<0.05）。与生理盐水组相比，Sulfasalazine 组的 MDA 和 PGF2α 水平显著降低（P<0.05，P<0.001）。与 PTZ+生理盐水组相比，Sulfasalazine 组的 SOD 明显升高（P<0.05）。本研究表明，Sulfasalazine 通过防止与 PTZ 相关的氧化和炎症损伤，对 PTZ 诱导的惊厥具有保护作用。
