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<p>Methylene blue (MB) is a neuroprotective agent with antioxidant properties. This study investigates the effects of MB on seizures, subsequent cognitive deficits and neuronal damage in a pentylenetetrazole (PTZ)-induced rat model of epilepsy. Rats were randomly divided into a Control group, an Epilepsy group (EP) and an MB intervention group (MB + EP). To induce kindling, the EP and MB + EP groups received intraperitoneal injections of PTZ (35&#xa0;mg/kg) once every other day for 15 total injections; the MB + EP group was pre-treated with MB (1&#xa0;mg/kg) 30&#xa0;min prior to each PTZ injection. Learning and memory were assessed using the Morris water maze (MWM) test. Hippocampal tissues were evaluated for neuronal survival via Nissl staining and for levels of malondialdehyde (MDA) and glutathione (GSH) via enzyme-linked immunosorbent assay. Compared with the EP group, MB intervention significantly reduced the full kindling rate (30.00% vs 84.62%, <i>P</i> = 0.0078), prolonged the latency to generalised tonic–clonic seizures (GTCS) (<i>P</i> = 0.0364) and shortened GTCS duration (<i>P</i> = 0.0231). Post-treatment assessments revealed that MB significantly attenuated neuronal loss in the hippocampal CA1 and CA3 regions (<i>P</i> &lt; 0.01) when compared with the EP group. Concurrently, it decreased hippocampal MDA levels (<i>P</i> &lt; 0.01) and increased GSH levels (<i>P</i> &lt; 0.01). Furthermore, in the MWM test, conducted 24&#xa0;h after the final injection, MB improved cognitive performance by shortening escape latency (<i>P</i> &lt; 0.01) and increasing platform crossings (<i>P</i> &lt; 0.05) compared with the EP group. Methylene blue demonstrates significant antiseizure and neuroprotective effects in a PTZ-induced epilepsy model. It likely alleviates seizure severity, protects hippocampal neurons and ameliorates cognitive dysfunction by mitigating oxidative stress, providing a strong experimental basis for its potential clinical use in treating epilepsy and its associated comorbidities.</p>

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Pretreatment With Methylene Blue Atenuates Seizures, Cognitive Impairment, Hippocampal Neuronal Damage and Oxidative Stress in Pentylenetetrazole-Kindled Rats

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Liping Jing,
  • Zhiqiang Cui,
  • Yan Luo,
  • Haoyun Zhang,
  • Yuqi Liu,
  • Yanli Yi

摘要

Methylene blue (MB) is a neuroprotective agent with antioxidant properties. This study investigates the effects of MB on seizures, subsequent cognitive deficits and neuronal damage in a pentylenetetrazole (PTZ)-induced rat model of epilepsy. Rats were randomly divided into a Control group, an Epilepsy group (EP) and an MB intervention group (MB + EP). To induce kindling, the EP and MB + EP groups received intraperitoneal injections of PTZ (35 mg/kg) once every other day for 15 total injections; the MB + EP group was pre-treated with MB (1 mg/kg) 30 min prior to each PTZ injection. Learning and memory were assessed using the Morris water maze (MWM) test. Hippocampal tissues were evaluated for neuronal survival via Nissl staining and for levels of malondialdehyde (MDA) and glutathione (GSH) via enzyme-linked immunosorbent assay. Compared with the EP group, MB intervention significantly reduced the full kindling rate (30.00% vs 84.62%, P = 0.0078), prolonged the latency to generalised tonic–clonic seizures (GTCS) (P = 0.0364) and shortened GTCS duration (P = 0.0231). Post-treatment assessments revealed that MB significantly attenuated neuronal loss in the hippocampal CA1 and CA3 regions (P < 0.01) when compared with the EP group. Concurrently, it decreased hippocampal MDA levels (P < 0.01) and increased GSH levels (P < 0.01). Furthermore, in the MWM test, conducted 24 h after the final injection, MB improved cognitive performance by shortening escape latency (P < 0.01) and increasing platform crossings (P < 0.05) compared with the EP group. Methylene blue demonstrates significant antiseizure and neuroprotective effects in a PTZ-induced epilepsy model. It likely alleviates seizure severity, protects hippocampal neurons and ameliorates cognitive dysfunction by mitigating oxidative stress, providing a strong experimental basis for its potential clinical use in treating epilepsy and its associated comorbidities.