Epilepsy is a chronic neurological condition that affects 1%–2% of the world population. Although research about the disease is advancing and a wide variety of drugs is available, about 30 % of patients have refractory epilepsy which cannot be controlled with the most common drugs. This highlights the need for a better understanding of the disorder and new types of treatment for it. Against this backdrop, a growing body of evidence has reported that inflammation may play a role both in the origin and in the progression of seizures. It has shown a tendency to be both the root and the result of epilepsy. This investigation aimed to assess the impact of prednisolone, a steroidal anti-inflammatory drug, in an animal model of pentylenetetrazole (PTZ)-induced seizures, at 1 mg/kg and 5 mg/kg doses. We also examined the degree of seizure severity and the modulation of pro-inflammatory cytokines in the treated animals. Four treatment groups were used (saline, diazepam, prednisolone 1 mg/kg, and prednisolone 5 mg/kg) and, in addition to their own daily treatments, subconvulsant doses of pentylenetetrazole (25 mg/kg) were administered every other day during a test protocol that lasted 14 days. After treatment, the cytokines interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) were measured in the animals’ sera, hippocampi, and prefrontal cortices. Animals treated with prednisolone presented less severe seizures than the animals in the saline group, and there was a decrease in pro-inflammatory cytokine levels in central structures, but not peripheral ones. In short, an animal model of chemically-induced epileptic seizures was used, in which the animals were treated with doses of prednisolone, and these animals presented less severe seizures than the negative control group (saline), in addition to showing decreased levels of pro-inflammatory cytokines IL-6, IL-1β and TNF-α, in the hippocampi and prefrontal cortices, but not the sera.

癫痫病是一种慢性神经系统疾病，影响了世界人口的1％–2％。尽管有关该疾病的研究正在推进，并且有各种各样的药物可供使用，但是约30％的患者患有难治性癫痫，这是最常见的药物无法控制的。这突出了需要更好地了解这种疾病及其新类型的治疗方法。在这种背景下，越来越多的证据表明炎症可能在癫痫发作的起源和发展中都起作用。它已显示出既是癫痫的根源又是结果的趋势。这项研究旨在评估泼尼松龙（甾体类抗炎药）在戊四唑（PTZ）诱发的癫痫发作动物模型中的作用，剂量为1 mg / kg和5 mg / kg。我们还检查了治疗动物的癫痫发作严重程度和促炎性细胞因子的调节。使用了四个治疗组（盐水，地西epa，泼尼松龙1 mg / kg和泼尼松龙5 mg / kg），除了他们自己的日常治疗外，在治疗期间每隔一天给予亚惊厥剂量的戊四氮（25 mg / kg）。测试方案，历时14天。治疗后，在动物的血清，海马和前额叶皮层中测量细胞因子白介素1β（IL-1β），白介素6（IL-6）和肿瘤坏死因子α（TNF-α）。与泼尼松龙治疗的动物相比，盐水组动物的癫痫发作严重程度要低，并且中央结构的促炎细胞因子水平降低，但周边结构没有降低。简而言之，