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BACKGROUND The aim of the present study was to investigate the potential anticonvulsant effect of methylene blue (MB) in a kainic acid (KA)-induced status epilepticus (SE) model. The effects of MB on levels of oxidative stress and glutamate (Glu) also were explored. MATERIAL AND METHODS Sixty C57BL/6 mice were randomly divided into 5 equal-sized groups: (1) controls; (2) KA; (3) MB 0.5 mg/kg+KA; (4) MB 1 mg/kg+KA; and (5) vehicle+KA. The SE model was established by intra-amygdala microinjection of KA. Behavioral observations and simultaneous electroencephalographic records of the seizures in different groups were analyzed to determine the potential anticonvulsant effect of MB. The influences of MB on oxidative stress markers and glutamate were also detected to explore the possible mechanism. RESULTS MB afforded clear protection against KA-induced acute seizure, as measured by the delayed latency of onset of generalized seizures and SE, decreased percentage of SE, and increased survival rate in mice with acute epilepsy. MB markedly increased the latency to first onset of epileptiform activity and decreased the average duration of epileptiform events, as well as the percentage of time during which the epileptiform activity occurred. Administration of MB prevented KA-induced deterioration of oxidative stress markers and Glu. CONCLUSIONS MB is protective against acute seizure in SE. This beneficial effect may be at least partially related to its potent antioxidant ability and influence on Glu level.

背景

本研究旨在探讨亚甲蓝（MB）在红藻氨酸（KA）诱导的癫痫持续状态（SE）模型中的潜在抗惊厥作用。还探讨了 MB 对氧化应激和谷氨酸（Glu）水平的影响。

材料和方法

60 只 C57BL/6 小鼠随机分为 5 组：（1）对照组；（2）KA 组；（3）MB0.5mg/kg+KA 组；（4）MB1mg/kg+KA 组；（5）载体+KA 组。通过内侧杏仁核内微量注射 KA 建立 SE 模型。分析不同组别的行为观察和同步脑电图记录，以确定 MB 的潜在抗惊厥作用。还检测了 MB 对氧化应激标志物和谷氨酸的影响，以探讨可能的机制。

结果

MB 对 KA 诱导的急性癫痫发作有明显的保护作用，表现为全身性发作和 SE 的发作潜伏期延迟、SE 百分比降低以及急性癫痫小鼠的存活率提高。MB 明显增加了癫痫样活动首次发作的潜伏期，并降低了癫痫样事件的平均持续时间以及癫痫样活动发生的时间百分比。MB 可预防 KA 诱导的氧化应激标志物和 Glu 恶化。