ObjectiveTo investigate the effects of hydrogen therapy on epileptic seizures in rats with refractory status epilepticus and the underlying mechanisms.MethodsStatus epilepticus was induced using pilocarpine. The effects of hydrogen treatment on epilepsy severity in model rats were then monitored using Racine scores and electroencephalography (EEG), followed by western blot of plasma membrane N-methyl-D-aspartate receptor subtype 2B (NR2B) and phosphorylated NR2B expression. We also generated a cellular epilepsy model using Mg2+-free medium and used polymerase chain reaction to investigate the neuroprotective effects of hydrogen.ResultsThere were no significant differences in Racine scores between the hydrogen and control groups. EEG amplitudes were lower in the hydrogen treatment group than in the control group. In epilepsy model rats, hippocampal cell membrane NR2B expression and phosphorylation increased gradually over time. Although hippocampal cell membrane NR2B expression was not significantly different between the two groups, NR2B phosphorylation levels were significantly lower in the hydrogen group. Hydrogen treatment also increased superoxide dismutase, mitochondrial (SOD2) expression.ConclusionsHydrogen treatment reduced EEG amplitudes and NR2B phosphorylation; it also decreased neuronal death by reducing oxidative stress. Hydrogen may thus be a potential treatment for refractory status epilepticus by inhibiting membrane NR2B phosphorylation and oxidative stress.

中文翻译：

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氢气治疗通过抑制膜 NR2B 磷酸化和氧化应激，减少难治性癫痫持续状态大鼠的脑电图活动和神经元死亡

目的探讨氢疗法对难治性癫痫持续状态大鼠癫痫发作的影响及其机制。方法采用毛果芸香碱诱导癫痫持续状态。然后使用拉辛评分和脑电图 (EEG) 监测氢气治疗对模型大鼠癫痫严重程度的影响，然后进行质膜 N-甲基-D-天冬氨酸受体亚型 2B (NR2B) 和磷酸化 NR2B 表达的蛋白质印迹。我们还使用 Mg 生成了细胞癫痫模型2+结果氢组和对照组的拉辛评分无显着差异。氢治疗组的脑电图振幅低于对照组。在癫痫模型大鼠中，海马细胞膜NR2B的表达和磷酸化随着时间的推移逐渐增加。尽管两组之间海马细胞膜NR2B表达没有显着差异，但氢组中NR2B磷酸化水平显着较低。氢气治疗还增加了超氧化物歧化酶、线粒体 (SOD2) 的表达。结论氢气治疗降低了 EEG 振幅和 NR2B 磷酸化；它还通过减少氧化应激来减少神经元死亡。因此，氢气可能通过抑制膜 NR2B 磷酸化和氧化应激来治疗难治性癫痫持续状态。