目的 探讨鹿茸多肽（VAP）对APP/PS1双转基因小鼠Rho/ROCK通路的影响。  方法 APP/PS1 双转基因小鼠随机分为模型组和鹿茸多肽组，每组 20只，另以同窝同性别阴性小鼠20只设立为对照组。鹿茸多肽组小鼠鹿茸多肽100 mg/kg灌胃给药，每天1次，连续28 d。治疗后水迷宫实验检测并记录小鼠逃避潜伏期和穿越平台次数；透射电子显微镜观察突触的超微结构；免疫荧光切片观察海马CA1区Ras同源基因家族成员A(RhoA)和Rho相关卷曲螺旋形成蛋白激酶Ⅱ（ROCKⅡ）的表达；Western blotting法检测海马内RhoA和ROCKⅡ蛋白相对表达量；ELISA法测定海马β-淀粉样蛋白（Aβ)1~42含量。  结果 与模型组比较，对照组和鹿茸多肽组逃避潜伏期均缩短，跨越平台次数增多。与模型组比较，对照组和鹿茸多肽组小鼠海马区突触计数增多，突触间隙宽度减小，突触后致密物厚度增加，差异有统计学意义(P＜0.05)。与模型组相比，对照组和鹿茸多肽组CA1区RhoA和ROCKⅡ表达量减少，Western blotting检测海马内RhoA和ROCKⅡ蛋白表达水平也减少(P＜0.05)。与模型组比较，对照组和鹿茸多肽组海马Aβ1~42含量均下降(P＜0.05)。  结论 鹿茸多肽对阿尔茨海默病模型小鼠神经损伤有保护作用，其机制可能通过抑制Rho/ROCK通路中RhoA和ROCKⅡ的表达，促进突触结构的改变和Aβ1~42含量减少，减轻神经损伤，改善认知功能。

Objective To study the effect of velvet antler polypeptides (VAP) on Rho/ROCK pathway in APP/PS1 double transgenic mice. 

  Methods APP/PS1 double transgenic mice were randomly divided into model group and velvet antler polypeptide group, 20 mice in each group, and control group consisting of 20 mice of the same litter and the same gender negative. The mice in VAP group were given velvet antler polypeptide 100 mg/kg by intragastric administration once a day for 28 days. After treatment, the water maze experiment was detected and recorded the escape latency and the number of crossing platforms of the mice; the ultrastructures of the synapse were observed by transmission electron microscopy; the expression of Rhs homolog gene family member A(RhoA) and Rho associated coiled-coil forming protein kinase Ⅱ(ROCKⅡ) in the hippocampal CA1 area were observed by immunofluorescence. The expression levels of RhoA and ROCKⅡ protein in the hippocampus were detected by Western blotting. The contents of hippocampus amyloid β-protein(Aβ)1-42 were determined by ELISA.   Results Compared with the model group, the escape latency was shortened, and the numbers of crossing platforms was increased in control group and VAP group. Compared with the model group, the synapse count in the hippocampus was increased, the width of the synaptic gap was decreased, and the thickness of the post-synaptic compact was increased in the control group and VAP group, the difference had significant(P＜0.05). Compared with the model group, the expression levels of RhoA and ROCKⅡ  in CA1 area reduced in control group and VAP group, and the expression levels of RhoA and ROCKⅡ protein in the hippocampus also reduced in control group and VAP group by Western blotting (P＜0-05).Compared with the model group, the contents of hippocampal Aβ1-42 in the control group and VAP group decreased.   Conclusion Velvet antler polypeptide has a protective effect on nerve damage in Alzheimer’s disease model mice, and its mechanism may promote the changes of synaptic structure and reduction of Aβ1-42 content, reduce nerve damage and improve cognitive function by inhibiting the expression of RhoA and ROCKⅡ in Rho/ROCK pathway.