Epilepsy is a neurological disease characterized by spontaneous and recurrent seizures. Epileptic seizures can be initiated and facilitated by inflammatory mechanisms. As the dysregulation of the immune system would be involved in epileptogenesis, it is suggested that anti-inflammatory medications could impact epileptic seizures. These medications could potentially have a side effect by altering the structure and composition of the intestinal microbiota. These changes can disrupt microbial homeostasis, leading to dysbiosis and potentially exacerbating intestinal inflammation. We hypothesize that prednisolone may affect the development of epileptic seizures, potentially influencing the diversity of the intestinal microbiota and the regulation of pro-inflammatory cytokines in intestinal tissue. This study aimed to evaluate the effects of prednisolone treatment on epileptic seizures and investigate the effect of this drug on the bacterial diversity of the intestinal microbiota and markers of inflammatory processes in intestinal tissue. We used Male Wistar rat littermates (n = 31, 90-day-old) divided into four groups: positive control treated with 2 mg/kg of diazepam (n = 6), negative control treated with 0.9 g% sodium chloride (n = 6), and the remaining two groups were subjected to treatment with prednisolone, with one receiving 1 mg/kg (n = 9) and the other 5 mg/kg (n = 10). All administrations were performed intraperitoneally (i.p.) over 14 days. To induce the chronic model of epileptic seizures, we administered pentylenetetrazole (PTZ) 25 mg/kg i.p. on alternate days. Seizure latency (n = 6 – 10) and TNF-α and IL-1β concentrations from intestinal samples were measured by ELISA (n = 6 per group), and intestinal microbiota was evaluated with intergenic ribosomal RNA (rRNA) spacer (RISA) analysis (n = 6 per group). The prednisolone treatment demonstrated an increase in the latency time of epileptic seizures and TNF-α and IL-1β concentrations compared to controls. There was no statistically significant difference in intestinal microbiota diversity between the different treatments. However, there was a strong positive correlation between microbial diversity and TNF-α and IL-1β concentrations. The administration of prednisolone yields comparable results to diazepam on increasing latency between seizures, exhibiting promise for its use in clinical studies. Although there were no changes in intestinal microbial diversity, the increase in the TNF-α and IL-1β cytokines in intestinal tissue may be linked to immune system signaling pathways involving the intestinal microbiota. Additional research is necessary to unravel the intricacies of these pathways and to understand their implications for clinical practice.

中文翻译：

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泼尼松龙在大鼠癫痫发作点燃模型中对细胞因子和肠道微生物群多样性的影响

癫痫是一种以自发性和反复发作为特征的神经系统疾病。炎症机制可以引发和促进癫痫发作。由于免疫系统失调与癫痫发生有关，因此建议抗炎药物可能会影响癫痫发作。这些药物可能会通过改变肠道微生物群的结构和组成而产生副作用。这些变化会破坏微生物稳态，导致生态失调并可能加剧肠道炎症。我们假设泼尼松龙可能会影响癫痫发作的发展，可能影响肠道微生物群的多样性和肠道组织中促炎细胞因子的调节。本研究旨在评估泼尼松龙治疗癫痫发作的效果，并研究该药物对肠道微生物群细菌多样性和肠道组织炎症过程标志物的影响。我们使用同窝雄性 Wistar 大鼠（n = 31，90 日龄）分为四组：用 2 mg/kg 地西泮处理的阳性对照（n = 6），用 0.9 g% 氯化钠处理的阴性对照（n = 6），其余两组接受泼尼松龙治疗，其中一组接受 1 mg/kg（n = 9），另一组接受 5 mg/kg（n = 10）。所有给药均通过腹膜内 (ip) 进行，历时 14 天。为了诱导癫痫发作的慢性模型，我们隔日腹腔注射戊四唑（PTZ）25 mg/kg。通过 ELISA 测量肠道样本的癫痫潜伏期 (n = 6 – 10) 以及 TNF-α 和 IL-1β 浓度（每组 n = 6），并通过基因间核糖体 RNA (rRNA) 间隔区 (RISA) 分析评估肠道微生物群（每组 n = 6）。与对照组相比，泼尼松龙治疗表明癫痫发作的潜伏时间以及 TNF-α 和 IL-1β 浓度有所增加。不同处理之间的肠道微生物群多样性没有统计学上的显着差异。然而，微生物多样性与 TNF-α 和 IL-1β 浓度之间存在很强的正相关性。在增加癫痫发作之间的潜伏期方面，泼尼松龙的给药与地西泮产生的结果相当，这显示出其在临床研究中的应用前景。尽管肠道微生物多样性没有变化，但肠道组织中TNF-α和IL-1β细胞因子的增加可能与涉及肠道微生物群的免疫系统信号通路有关。需要进行更多的研究来阐明这些途径的复杂性并了解它们对临床实践的影响。