目的 建立丙戊酸钠(valproic acid,VPA)孤独症动物模型,观察核转录因子κB和小清蛋白阳性神经元在VPA孤独症模型鼠海马CA1区的表达,探讨孤独症可能的发病机制,为完善其治疗方案提供理论依据。方法 按Schneider方法制作VPA孤独症动物模型,采用免疫组化和图像分析技术检测孤独症模型鼠海马CA1区核转录因子κB和小清蛋白阳性神经元的表达。结果 与正常对照组比较,孤独症模型组海马CA1区核转录因子κB阳性神经元数目增加(4.67±1.56 vs 3.00±1.54,t=2.639,P=0.015);海马CA1区小清蛋白表阳性神经元数目增加(5.33±0.99 vs 2.83±1.27,t=5.378,P=0.000)。结论 孤独症的发病可能与海马CA1区核转录因子κB和小清蛋白的表达水平有关。
Abstract
Objective To establish the animal model of autism and explore pathogenesis of autism by observation of changes of nuclear factor-kappa B (NF-κB) and parvalbumin(PV) positive neurons in hippocampal CA1 region and to provide theoretical evidence for the therapeutic schedule of autism. Methods Animal model of autism was obtained as Schneider showed.The immunohistochemistry methods and image analysis were used to examine the number of NF-κB,and PV positive neurons in hippocampal CA1 region in autism model rats and the normal rats. Results The number of NF-κB positive neurons in the hippocampal CA1 region of the autism model rats was more than that of the normal rats(4.67±1.56 vs 3.00±1.54,t=2.639,P=0.015).The number of PV positive neurons in the hippocampal CA1 region of the autism model rats was more than that of the normal rats (5.33±0.99 vs 2.83±1.27,t=5.378,P=0.000). Conclusion The occurrence of autism may be related to the changes of NF-κB and PV in hippocampal CA1 region.
关键词
孤独症谱系障碍 /
核转录因子κB /
小清蛋白 /
丙戌酸钠 /
大鼠
Key words
autism spectrum disorder /
nuclear factor-kappa B /
parvalbumin /
valproic acid /
rats
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基金
青岛大学医学院附属医院2010年重点培育学科专项建设基金(2010-610)
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