补肾法中药调控ERK/MAPK信号通路对Aβ25-35诱导的阿尔茨海默病大鼠模型的神经保护作用研究Neuroprotective Study of Tonifying Kidney TCM Drugs in Aβ25-35-induced Alzheimer′s Disease in Rat Model by Regulating ERK/MAPK Signaling Pathway
刘爽;徐家淳;孙伟明;曹艺萌;王以申;
摘要(Abstract):
目的 观察补肾法中药通过调控ERK/MAPK信号通路关键靶点蛋白,探讨其对Aβ25-35诱导的阿尔茨海默病(AD)大鼠模型的神经保护作用机制。方法 取36只雌性SD大鼠随机分为假手术组、模型组、中药组,每组12只。采用Aβ25-35侧脑室注入建立AD大鼠模型,中药组予补肾中药,模型组及假手术组予蒸馏水灌胃,观察各组大鼠认知记忆能力、海马神经元凋亡、p-ERK1/2蛋白表达情况。结果 1)AD认知记忆功能检测:与模型组相比,中药组大鼠定位航行实验显示,平均速度无显著差异(P> 0.05),潜伏时间明显缩短,学习能力明显上升,差异具有统计学意义(P <0.05)。2)AD海马神经元凋亡检测:光镜下观察尼氏染色结果显示,与模型组相比,中药组神经元凋亡数量明显减少(P <0.01)。3)ERK/MAPK信号通路关键靶点p-ERK1/2蛋白表达的检测:Western blotting检测结果显示,与假手术组相比,模型组p-ERK1/2蛋白的表达均明显降低,差异具有统计学意义(P <0.05);与模型组相比,中药组p-ERK1/2蛋白的表达明显增加,差异具有统计学意义(P <0.05)。结论 补肾法中药对Aβ25-35诱导的AD模型大鼠海马神经元损伤具有保护作用,可明显改善AD模型大鼠认知和记忆能力,减少海马神经元的凋亡,其作用机制可能调控p-ERK1/2蛋白表达,激活ERK/MAPK信号通路有关。
关键词(KeyWords): 老年性痴呆;阿尔茨海默病;补肾法;ERK/MAPK信号通路;大鼠
基金项目(Foundation): 国家自然科学基金面上基金项目(81973797);; 天津市教委科研计划项目(2021ZD023)
作者(Authors): 刘爽;徐家淳;孙伟明;曹艺萌;王以申;
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