Abstract

Epilepsy is a disease characterized by recurrent and unprovoked seizures. Cognitive deficiency and anxiety are important comorbidities of the chronic epilepsy. Studies on epilepsy using human and animal models have shown that aerobic exercise (AX) induces beneficial structural and functional changes and reduce the intensity of seizures. The present study seeks to evaluate effects of an AX program on the intensity of seizures, cognitive function and anxiety-like behavior and expression of serum brain-derived neurotrophic factor (BDNF) level in mice with epilepsy. The intensity of seizures was recorded 30 min following pentylenetetrazol (PTZ) injection, and cognitive function and anxiety-like behavior were assessed through novel object recognition task (NORT) and light–dark box test, respectively. Using ELISA, the effects of AX program on the serum BDNF level of epileptic mice was further determined. Mice with epilepsy subjected to AX showed a reduction in the intensity of seizures compared to non-exercised epileptic mice. Memory deficits and increased anxiety-like behavior were attenuated by AX which also restored the Serum BDNF level, reduced in epileptic mice, to control levels. In conclusion, AX reduces seizure intensity and mitigates memory deficits and increased anxiety-like behavior in mice with epilepsy. These AX induced beneficial effects can be ascribed to the changes in BDNF level. Finally, AX might be as a complementary therapeutic strategy for treating epilepsy.

中文翻译：

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通过增加慢性癫痫小鼠的BDNF，通过有氧运动减少癫痫发作强度并减轻记忆缺陷和焦虑感行为

摘要

癫痫病是以反复发作和无故发作为特征的疾病。认知不足和焦虑是慢性癫痫的重要合并症。使用人和动物模型进行的癫痫病研究表明，有氧运动（AX）会引起有益的结构和功能变化，并降低癫痫发作的强度。本研究旨在评估AX程序对癫痫小鼠癫痫发作强度，认知功能和焦虑样行为以及血清脑源性神经营养因子（BDNF）表达的影响。注射戊四氮（PTZ）后30分钟记录癫痫发作的强度，并分别通过新型物体识别任务（NORT）和明暗盒测试评估认知功能和焦虑样行为。使用ELISA，进一步确定了AX程序对癫痫小鼠血清BDNF水平的影响。与未锻炼的癫痫小鼠相比，患有AX癫痫的小鼠的癫痫发作强度降低。AX减弱了记忆缺陷和焦虑样行为的增加，这也将血清BDNF水平（在癫痫小鼠中降低）恢复至对照水平。总之，AX可以降低癫痫小鼠的癫痫发作强度并减轻记忆缺陷和增加类似焦虑的行为。这些AX诱导的有益作用可归因于BDNF水平的变化。最后，AX可能作为治疗癫痫的补充治疗策略。AX减弱了记忆缺陷和焦虑样行为的增加，这也将血清BDNF水平（在癫痫小鼠中降低）恢复至对照水平。总之，AX可以降低癫痫小鼠的癫痫发作强度并减轻记忆缺陷并增加焦虑样行为。这些AX诱导的有益作用可归因于BDNF水平的变化。最后，AX可能作为治疗癫痫的补充治疗策略。AX减弱了记忆缺陷和焦虑样行为的增加，这也将血清BDNF水平（在癫痫小鼠中降低）恢复至对照水平。总之，AX可以降低癫痫小鼠的癫痫发作强度并减轻记忆缺陷并增加焦虑样行为。这些AX诱导的有益作用可归因于BDNF水平的变化。最后，AX可能作为治疗癫痫的补充治疗策略。