山奈酚对外伤性癫痫大鼠治疗作用及机制研究

Therapeutic effect and mechanism of kaempferol on traumatic epilepsy in rats

目的:探究山奈酚对外伤性癫痫大鼠治疗作用及机制。方法:利用随机数法将实验大鼠随机分为三组,癫痫组在大鼠大脑的体感区注射FeCl_(3)建立外伤性癫痫模型,对照组给予等量0.9%氯化钠注射液,山奈酚组在大鼠侧脑室内注射20 mg/(kg·d)山奈酚。利用脑电图仪检测大鼠脑电波,利用水迷宫和抬高迷宫实验检测大鼠空间学习和记忆能力,利用组织切片染色评估大鼠海马组织结构,利用试剂盒检测大鼠脑组织氧化应激和炎症指标,利用免疫印迹技术检测相关通路蛋白表达水平。结果:在大鼠大脑的体感区注射FeCl_(3)成功构建了外伤性癫痫模型;山奈酚能够提高癫痫大鼠的空间学习和记忆能力(均P<0.05);山奈酚缓解了癫痫大鼠海马组织的变性损伤;山奈酚降低了癫痫大鼠脑组织的氧化应激和炎性反应(均P<0.05);山奈酚降低了癫痫大鼠脑组织磷酸化的P38蛋白和细胞外调节蛋白激酶含量(均P<0.05)。结论:山奈酚可能通过抑制P38和细胞外调节蛋白激酶通路活化减轻海马组织的氧化应激和炎性反应,从而缓解大鼠外伤性癫痫。

Objective:To explore the therapeutic effect and mechanism of kaempferol on traumatic epilepsy in rats.Methods:The experimental rats were randomly divided into three groups by random number method.The rats in epileptic group were injected FeCl_(3) into the brain somatosensory area to establish the traumatic epilepsy model,while the control group was given 0.9%sodium chloride injection.In the kaempferol group,20 mg/(kg·d)kaempferol was injected into the lateral ventricle of rats.The electroencephalograph was used to detect the brain wave of rats.The water maze and elevation maze experiments were used to test the spatial learning and memory abilities of rats.The tissue structure of rat hippocampus was evaluated by tissue section staining.The kit was used to detect oxidative stress and inflammation indicators in rat brain tissue.The expression of related pathway proteins were detected by Western blot.Results:The traumatic epilepsy model was successfully constructed by injecting FeCl_(3) into the rain somatosensory area of rats.Kaempferol improved the spatial learning and memory ability of epileptic rats(all P<0.05).Kaempferol alleviated the degeneration damage of hippocampal tissue in epileptic rats.Kaempferol reduced oxidative stress and inflammatory reaction in brain tissue of epileptic rats(all P<0.05).Kaempferol reduced the levels of phosphorylated P38 protein and extracellular regulated protein kinase(ERK)in brain tissue of epileptic rats(all P<0.05).Conclusion:Kaempferol may reduce oxidative stress and inflammatory response in hippocampus by inhibiting the activation of P38 and extracellular regulatory protein kinase pathway,thus alleviating traumatic epilepsy in rats.