Noggin蛋白对D-半乳糖致衰老小鼠学习记忆及海马齿状回神经发生的影响

目的观察侧脑室注射Noggin蛋白后对D 半乳糖致衰老模型小鼠学习记忆行为能力与海马齿状回神经发生的影响。方法采用皮下注射D 半乳糖构建衰老小鼠模型后,连续7?d侧脑室注射Noggin蛋白,对照组同时注射等量生理盐水,造模42?d后对各组小鼠进行Y迷宫学习记忆能力测试,用BrdU标记海马齿状回增殖细胞。 结果Y迷宫检测结果表明,模型组小鼠学习记忆能力较正常对照组明显降低（P<0.05）,而模型治疗组小鼠学习记忆能力较模型对照组明显改善（P<0.05）;模型组与模型对照组小鼠海马齿状回BrdU阳性细胞数较正常对照组减少（P<0.05）,而模型治疗组BrdU阳性细胞数较模型组、模型对照组显著增多（P<0.05）。结论侧脑室给予Noggin蛋白可改善衰老模型小鼠的空间学习及记忆能力,可能与Noggin能保护海马神经元并促使齿状回神经干细胞增殖有关。   

Effect of intracerebroventricular injection of noggin on learning and memory and neurogenesis in hippocampal dentate gyrus of D-galactose induced aging mice

To investigate endogenous neurogenesis and learning and memory in hippocampul dentate gyrus of D galactose induced aging mice by intracerebroventricular injection of noggin protein. Method40 mature KM male mice were randomly divided into the normal control group, the aging model group, the treatment control group and the noggin treatment group. In the aging model group, treatment control group and treatment group, D galactose (125?mg·kg-1·d-1)  was given to mice for 6 weeks by subcutaneous injection. Noggin protein was injected into the lateral cerebral ventricle for 7 days after 6 weeks in the noggin treatment group, and saline was injected into the lateral cerebral ventricle in the treatment control group. Learning and memory abilities were measured by a Y maze test 7 days after the operation. Neurogenesis was observed with BrdU immunohistochemical staining and the number of BrdU positive cell were statistically analyzed in the hippocampal dentate gyrus. ResultsLearning and memory abilities in the aging control group were significantly decreased compared with the normal control group (P<0.05) but in the noggin treatment group were significantly increased compared with the aging model group and treatment control group (P<0.05). BrdU positive neurons in the noggin treatment group were increased compared with the aging control group and treatment control group (P<0.05). ConclusionNoggin protein can improve learning and memory abilities of the aging model mice, which may be related to D galactose inducing impairment of neurogenesis and enhancing neurogenesis in the hippocampal dentate gyrus.