孤独症谱系障碍（ASD）是一种广泛性儿童神经发育疾病，其发病机制未明且缺乏有效药物干预。ASD患者脑内存在大量冗余突触提示胶质细胞的突触修剪功能异常可能是ASD的重要发病机制。研究表明ASD患者脑内广泛存在大量活化的小胶质细胞与星形胶质细胞，过度活化的胶质细胞大量释放促炎症细胞因子可能使其突触修剪功能受损从而导致ASD。临床研究显示萝卜硫素（SFN）能显著改善ASD症状，但其作用机制未明。研究证实SFN能激活Nrf2阻断NF-κB炎症通路。所以我们推测SFN激活Nrf2阻断胶质细胞的NF-κB炎症通路抑制胶质细胞活化后可能调控其突触修剪功能发挥治疗ASD的作用。本研究将首先建立基于胶质细胞过度激活的ASD大鼠模型，在活体水平研究SFN干预ASD的疗效，再用ASD大鼠脑组织切片和体外急性脑片模型，在细胞和分子水平上研究SFN激活Nrf2阻断胶质细胞NF-κB通路调控突触修剪功能的作用。

Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder. The pathogensis of ASD have not been understood and there is no approved medical therapy addresses core symptoms of ASD. Excessive synapse found in the brain of children with ASD suggested errant glial-cell dependent synaptic pruning may have played a role in the pathogenesis of ASD. Also, brain samples showed increased reactive glial cells in ASD. Therefore, overreacted glial cells may release a number of neuroactive proinflammatory factors and exacerbate the inflammatory condition and contribute to insufficient synaptic pruning in the brain that resulted in ASD. A recent clinical trial showed that sulforaphane (SFN) treatment significantly improved core symptoms of ASD, with unclear mechanism. In addition, studies have reported that SFN may inhibit the nuclear factor-κB (NF-κB) proinflammatory pathway by activating Nrf2. Therefore, we speculate that the treatment effect of SFN on ASD may be mediated through its inhibition of NF-κB pathway and regulate synaptic pruning functions of glial cells by suppressing its overreaction in inflammatory condition. This study will firstly evaluate the treatment effect of ASD on ASD rat models and secondly verify SFN activate Nrf2 and inhibite NF-κB pathways and its association with synaptic pruning functions of glial cells.