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姜黄素和脑源性神经营养因子对阿尔茨海默病记忆的改善作用
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姜黄素和脑源性神经营养因子对阿尔茨海默病记忆的改善作用
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Journal Article
姜黄素和脑源性神经营养因子对阿尔茨海默病记忆的改善作用
2016
Overview
目的研究姜黄素对阿尔茨海默病（Alzheimer＇s disease,AD）模型大鼠学习记忆能力的影响及其作用机制。方法采用脑室内注射Aβ1-42的方法,制备AD动物模型。单次腹腔注射（急性治疗组）或连续6d腹腔注射（慢性治疗组）50、100、300mg/kg剂量的姜黄素,结合海马内微量注射脑源性神经营养因子（brain-derived neurotrophic factor,BDNF）（每侧1.0μg）、BDNF shRNA慢病毒（每侧2.0×105单位）,分析大鼠Y迷宫、Morris水迷宫及旷场行为变化,并应用Western blot检测海马BDNF表达变化。结果姜黄素急性治疗对AD模型大鼠自主改变行为、总活动距离、水迷宫潜伏期没有显著作用。300mg/kg姜黄素慢性治疗后AD大鼠自主改变行为（P〈0.000 1）及在水迷宫测试中记忆能力（P〈0.05）比盐水对照组显著增高。100和300mg/kg姜黄素慢性治疗组海马BDNF表达和盐水对照组相比显著上升（P分别〈0.05和〈0.000 1）。海马内注射BDNF的AD大鼠水迷宫潜伏期显著下降（F_（4,295）=5.813,P〈0.01）。姜黄素慢性治疗＋shBDNF组大鼠在2号象限内的游泳时间与盐水对照组无差异（P=0.657）,而100mg/kg姜黄素组、BDNF组、假手术组大鼠的停留时间比盐水对照组显著增高（P值分别〈0.05、〈0.05、〈0.000 1）。结论姜黄素可能通过上调BDNF的表达继而激活下游信号通路,最终对Aβ诱导的AD大鼠学习记忆能力起到改善作用。
