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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±1.56vs 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±0.99vs 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。
Objective To establish an autistic animal model of valproic acid (VPA) and observe the expression of nuclear factor-κB and small-albumin-positive neurons in the CA1 region of hippocampus of VPA autism model mice and explore the possible pathogenesis of autism Improve its treatment program to provide a theoretical basis. Methods According to the method of Schneider, autistic animal model of VPA was established. The expression of nuclear factor kappa B (NF-κB) and small-albumin-positive neurons in hippocampal CA1 area of autism model mice were detected by immunohistochemistry and image analysis. Results Compared with the normal control group, the number of nuclear factor kappa B positive neurons in hippocampal CA1 region in autism model group increased (4.67 ± 1.56 vs 3.00 ± 1.54, t = 2.639, P = 0.015) The number of elements increased (5.33 ± 0.99 vs. 2.83 ± 1.27, t = 5.378, P = 0.000). Conclusion The incidence of autism may be related to the expression of nuclear factor kappa B and small albumin in CA1 area of hippocampus.