[1]冯娇娇,邢雅杰,刘丹丹.基于p38 MAPK/NF-κB信号通路探究茯苓多糖对癫痫模型小鼠癫痫发作情况、神经元损伤及炎症反应的影响[J].卒中与神经疾病杂志,2024,31(05):494-498.[doi:10.3969/j.issn.1007-0478.2024.05.013]
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基于p38 MAPK/NF-κB信号通路探究茯苓多糖对癫痫模型小鼠癫痫发作情况、神经元损伤及炎症反应的影响()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第31卷
期数:
2024年05期
页码:
494-498
栏目:
论著
出版日期:
2024-10-20

文章信息/Info

文章编号:
1007-0478(2024)05-0494-05
作者:
冯娇娇邢雅杰刘丹丹
056001 河北省邯郸市中心医院(冯娇娇 刘丹丹); 邯郸市第一医院(邢雅杰)
关键词:
茯苓多糖 癫痫 小鼠 神经元损伤 炎症反应 p38丝裂原活化蛋白激酶 核转录因子-κB
分类号:
R742.1
DOI:
10.3969/j.issn.1007-0478.2024.05.013
文献标志码:
A
摘要:
目的 探究茯苓多糖对癫痫模型小鼠癫痫发作情况、神经元损伤、炎症反应及p38丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)/核转录因子-κB(Nuclear transcription factor-κB,NF-κB)信号通路的影响。方法 构建癫痫小鼠模型,将60只癫痫模型小鼠随机分为模型组、茯苓多糖低(3 mg/kg)、中(6 mg/kg)、高(12 mg/kg)剂量组、卡马西平(30 mg/kg)组,12只/组,另取12只健康小鼠作为对照组; 各组小鼠连续14 d灌胃相应药物(1次/d); 于给药周期完成后24 h记录1 d内8:00-20:00癫痫发作次数和平均持续时间; 苏木精-伊红及原位末端标记法(TdT-mediated dUTP nick and labeling,TUNEL)染色分别观察海马组织病理学及神经元凋亡情况; 酶联免疫吸附及蛋白印迹法分别检测海马组织白细胞介素(Interleukin,IL)-1β、IL-6、肿瘤坏死因子(Tumor necrosis factor,TNF)-α及p38丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)、核转录因子-κB(Nuclear transcription factor-κB,NF-κB)蛋白水平。结果 与对照组比较,模型组海马组织神经元排列稀疏紊乱、体积缩小、核固缩,癫痫发作次数、平均持续时间、海马组织神经元凋亡率、IL-1β,IL-6,TNF-α,p38 MAPK、NF-κB蛋白水平显著升高(P<0.05); 与模型组比较,茯苓多糖低、中、高剂量组海马组织神经元病理损伤程度逐渐减轻,癫痫发作次数、平均持续时间、海马组织神经元凋亡率、IL-1β,IL-6,TNF-α,p38 MAPK,NF-κB蛋白水平呈剂量依赖性降低(P<0.05); 卡马西平组海马组织神经元病理损伤程度及各项指标水平变化与茯苓多糖高剂量组无显著差异(P>0.05)。结论 茯苓多糖可减少癫痫模型小鼠癫痫发作情况,减轻海马组织神经元损伤及炎症反应,抑制p38 MAPK/NF-κB信号通路活性可能是其作用机制之一。

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备注/Memo

备注/Memo:
基金项目:河北省医学科学研究课题计划项目(编号为20230455)
更新日期/Last Update: 2024-10-20