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目的观察孤独症大鼠前额叶皮质神经元凋亡相关蛋白Caspase-3和Bcl-2表达的变化,探讨细胞凋亡在孤独症发病中的作用。方法健康繁殖期Wistar雌鼠20只,体质量250~260 g,随机选取10只在E12.5腹腔注射丙戊酸钠(VPA),其子代为孤独症模型组;其余10只在E12.5腹腔注射生理盐水,其子代为对照组。通过比较负向性实验、自梳理实验验证模型是否成功;Western blotting方法对比对照组与孤独症模型组大鼠P42前额叶皮质凋亡相关蛋白Caspase-3和Bcl-2表达的变化。结果成功建立孤独症动物模型。与对照组比较,孤独症模型组大鼠旋转调头时间显著延长(P<0.05),理毛时间显著增加(P<0.05);P42前额叶皮质凋亡相关蛋白Caspase-3表达显著降低(P<0.05),Bcl-2表达显著升高(P<0.05)。结论孤独症大鼠P42前额叶皮质凋亡受到抑制,提示调节凋亡可能是一个潜在的孤独症治疗策略。
Objective To observe the changes of apoptosis-related proteins Caspase-3 and Bcl-2 in the prefrontal cortex of autistic rats and to explore the role of apoptosis in the pathogenesis of autism. Methods Twenty healthy Wistar female mice were breeded with 250-260 g body weight. Ten randomly selected mice were injected intraperitoneally with sodium valproate (VPA) at E12.5, and their offsprings were autistic model group. The other ten were randomly divided into two groups: E12.5 Intraperitoneal injection of saline, the offspring of the control group. By comparing the negative experiment, the model was verified by combing experiments; Western blotting was used to compare the expression of Caspase-3 and Bcl-2 in the P42 prefrontal cortex in the control group and autism model group. Results The autistic animal model was successfully established. Compared with the control group, the rotation time of rats in autism model group was significantly prolonged (P <0.05), the time of grooming was significantly increased (P <0.05), and the expression of Caspase-3 in P42 prefrontal cortex significantly decreased (P < 0.05). The expression of Bcl-2 was significantly increased (P <0.05). Conclusions The apoptosis of P42 prefrontal cortex is inhibited in autistic rats, suggesting that regulation of apoptosis may be a potential treatment strategy for autism.