Rahimi-Tesiye Maryam, Rajabi-Maham Hassan, Hosseini Abdolkarim, Azizi Vahid
Department of Animal Sciences and Marine Biology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran.
Department of Animal Sciences and Marine Biology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran.
Brain Res Bull. 2025 Jan;220:111151. doi: 10.1016/j.brainresbull.2024.111151. Epub 2024 Dec 1.
Hippocampal-dependent cognitive impairments are consequences of temporal lobe epilepsy. This study aimed to assess the modulatory effects of fenoprofen on Pentylenetetrazol (PTZ)-induced cognitive dysfunction in the rat model of epilepsy. Male Wistar rats were randomly divided into five groups. Except for the control group, the kindling model was induced by intraperitoneal (IP) injection of PTZ (35 mg/kg) every other day for a month. Three groups received fenoprofen (10, 20, and 40 mg/kg) before each PTZ injection. One week after kindling development, rats were challenged with PTZ (70 mg/kg). The Morris Water Maze, Shuttle Box, and Elevated Plus Maze tests were applied to assess cognitive functions. Rats' serum and brain samples were prepared for biochemical, histological, and gene expression studies. Fenoprofen pretreatment effectively reduced the mean seizure score, and treated rats had better cognitive performance than the PTZ group in passive avoidance and spatial memory and learning tests; they also showed less anxiety-like behaviors. Its administration also showed anti-oxidative properties. So the serum level of Nitric oxide was significantly reduced while Glutathione and Catalase increased significantly. It also diminished the expression of inflammatory genes (Tumor Necrosis Factor alpha (TNF-α) and Nuclear Factor Kappa B (NF-kB)) in the hippocampus, these results were confirmed by histological observation from Hematoxylin & Eosin staining. These results show the ability of fenoprofen to reduce cognitive impairments caused by epilepsy induction. These effects seem to be through the modulation of inflammatory mediators and oxidative stress.
海马体依赖性认知障碍是颞叶癫痫的后果。本研究旨在评估非诺洛芬对癫痫大鼠模型中戊四氮（PTZ）诱导的认知功能障碍的调节作用。雄性Wistar大鼠被随机分为五组。除对照组外，每隔一天腹腔注射PTZ（35毫克/千克）诱导点燃模型，持续一个月。三组在每次注射PTZ前接受非诺洛芬（10、20和40毫克/千克）。点燃模型建立一周后，用PTZ（70毫克/千克）对大鼠进行刺激。应用莫里斯水迷宫、穿梭箱和高架十字迷宫试验评估认知功能。制备大鼠血清和脑样本用于生化、组织学和基因表达研究。非诺洛芬预处理有效降低了平均癫痫发作评分，在被动回避、空间记忆和学习测试中，治疗组大鼠的认知表现优于PTZ组；它们还表现出较少的焦虑样行为。其给药还显示出抗氧化特性。因此，一氧化氮的血清水平显著降低，而谷胱甘肽和过氧化氢酶显著增加。它还减少了海马体中炎症基因（肿瘤坏死因子α（TNF-α）和核因子κB（NF-κB））的表达，苏木精和伊红染色的组织学观察证实了这些结果。这些结果表明非诺洛芬具有减轻癫痫诱导所致认知障碍的能力。这些作用似乎是通过调节炎症介质和氧化应激来实现的。
