大脑衍生的神经营养因子水平和自闭症中的氧化压力:来自儿童和小鼠模型的证据
Xiaozhuang Zhang1, Chenghui Fu1, Min Wang1
1From the Hainan Women and Children's Medical Center, Hainan Medical University (Zhang, Fu, M. Wang, Feng, H. Wang, H. Li, L. Li, Yao); Department of Gynecology, The Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen China (Liu, Zeng).
Journal of psychiatry & neuroscience : JPN
|July 25, 2025
概括
在自闭症谱系障碍 (ASD) 中,外围大脑衍生神经营养因子 (BDNF) 的升高与氧化压力有关. 在小鼠模型中调节超氧化物脱酶2 (SOD2) 逆转了这些变化,并减少了类似自闭症的行为.
科学领域:
- 神经科学是一个神经科学.
- 发展生物学 发展生物学
- 遗传学 是一个遗传学.
背景情况:
- 大脑衍生神经营养因子 (BDNF) 在神经发育中起着至关重要的作用,并与自闭症谱系障碍 (ASD) 有关.
- 在ASD中,外围BDNF水平是可变的,它们与氧化应激的关系尚未完全理解.
研究的目的:
- 研究患有自闭症儿童的循环氧化应激和外围BDNF水平之间的关联.
- 在临床前模型中探索调节氧化还原平衡对BDNF水平和自闭症类行为的影响.
主要方法:
- 分析了ASD儿童的血BDNF和氧化还原状态,以及典型发育 (TD) 对照.
- 利用小鼠模型的ASD诱导的产前暴露于medroxyprogesterone乙酸 (MPA).
- 采用超氧化物脱酶2 (SOD2) 和血造干细胞 (HSC) 移植的lentiviral表达来调节小鼠模型中的氧化还原平衡.
主要成果:
- 与TD对照组相比,患有ASD的儿童表现出血BDNF升高和改变的氧化还原平衡.
- 暴露于MPA的小鼠表现出外围BDNF和氧化应激的增加.
- 在小鼠模型中的SOD2调制使BDNF水平正常化,并减轻了类似自闭症的行为.
结论:
- 在ASD中增加的外周BDNF与循环氧化应激相关.
- 产前孕激素暴露有助于增加BDNF和氧化应激,这可以通过SOD2调制逆转.
- 研究结果表明,通过解决氧化应激和BDNF通路,ASD是一种潜在的治疗点.
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