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天麻素对癫痫大鼠海马神经元IL-1β、TNF-α及IL-10的影响

发布时间:2018-08-07 11:35
【摘要】:目的探讨IL-1β、TNF-α及IL-10在癫痫发病中的作用以及天麻素对癫痫大鼠海马神经元IL-1β、TNF-α及IL-10水平的影响。方法将45只成年雄性Wistar大鼠随机分为正常对照组(NC组)15只、癫痫组(EP组)15只和天麻素组(GE组)15只。EP组和GE组每日1次经腹腔注射阈下剂量的戊四氮建立大鼠癫痫模型,然后给予GE组大鼠腹腔注射天麻素,观察两组大鼠的行为学变化。应用免疫组织化学的方法检测大鼠海马IL-1β、TNF-α及IL-10水平的变化并进行比较。结果 GE组的发作潜伏期较EP组明显延长,且发作持续时间缩短、发作强度降低(P0.05)。EP组与NC组比较,大鼠海马神经元IL-1β、TNF-α水平明显上调(P0.01),而IL-10水平明显降低(P0.01)。GE组与EP组比较,大鼠海马神经元IL-1β、TNF-α水平明显降低(P0.01),而IL-10水平明显升高(P0.01)。结论 IL-1β、TNF-α可促进癫痫的发生与发展,而IL-10有抗癫痫作用;天麻素可通过降低IL-1β、TNF-α水平并升高IL-10而发挥抗癫痫作用。
[Abstract]:Objective to investigate the role of IL-1 尾 -TNF- 伪 and IL-10 in the pathogenesis of epilepsy and the effect of Gastrodin on the levels of IL-1 尾 -TNF- 伪 and IL-10 in hippocampal neurons of epileptic rats. Methods Forty-five adult male Wistar rats were randomly divided into normal control group (NC group, n = 15), epilepsy group (EP group, n = 15), Gastrodin group (GE group, n = 15) and GE group (n = 15). Then the rats in GE group were given Gastrodin intraperitoneally to observe the behavioral changes of the two groups. The changes of IL-1 尾 -TNF- 伪 and IL-10 in hippocampus of rats were detected by immunohistochemical method and compared. Results compared with NC group, the latency of attack in GE group was significantly prolonged, the duration of attack was shortened and the intensity of attack was decreased (P0.05). Compared with NC group, the level of IL-1 尾 -TNF- 伪 in hippocampal neurons in group GE was significantly up-regulated (P0.01), while the level of IL-10 in group GE was significantly lower than that in group EP (P0.01). The level of IL-1 尾 -TNF- 伪 in hippocampal neurons decreased significantly (P0.01), while the level of IL-10 increased significantly (P0.01). Conclusion IL-1 尾 -TNF- 伪 can promote the occurrence and development of epilepsy, while IL-10 has antiepileptic effect, Gastrodin can play an antiepileptic effect by decreasing the level of IL-1 尾 -TNF- 伪 and increasing IL-10.
【作者单位】: 长江大学医学院附属荆州市第一人民医院神经内科;
【分类号】:R742.1

【参考文献】

相关期刊论文 前2条

1 赵燕玲;张博爱;贾延R,

本文编号:2169894


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