Li Jing, Chai Xuejun, Song Dongfeng, Wang Mengli, Sun Penghao, Zhao Yongkang, Ren Duoduo, Liu Feng, Ni Hong, Jiang Yonghong, Zhu Xiaoyan, Li Enyao, Zhao Shanting
College of Veterinary Medicine, Northwest A&F University, Yangling, China.
College of Basic Medicine, Xi'an Medical University, Xi'an, China.
Food Funct. 2025 Jul 14;16(14):5771-5790. doi: 10.1039/d4fo06180b.
Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social communication and repetitive behaviours. The gut microbiota plays a pivotal role in the etiology of autism spectrum disorder, and its modulation represents a promising therapeutic strategy to alleviate autism-like behaviours. The purpose of this study was to evaluate the effects of oil (ASO) on autism-like behaviours in an autistic mouse model, BTBR T Itpr3/J (BTBR) mice, and to assess the related molecular mechanisms. The juvenile BTBR mice were administered with ASO for 36 consecutive days by gavage. Behaviour tests showed that ASO remarkably alleviated the autism-like behaviours of BTBR mice. In addition, the supplementation with ASO promoted the maturation of oligodendrocytes and suppressed microglial over-activation, and reduced the IL-1β and TNF-α levels in the hippocampus of the BTBR mice. Oral ASO administration also improved gut microbiota imbalances in BTBR mice by reducing the abundance of the harmful bacterium and the ratio of to . Additionally, ASO decreased the expression of TNF-α and IL-1β, and increased the levels of ZO-1, claudin-1 and occludin in the intestine, thereby reducing intestinal inflammation and repairing intestinal barrier damage. Our results indicate that ASO has great potential in the treatment of autism, providing theoretical basis for the development of autism drugs.
自闭症谱系障碍（ASD）是一种复杂的神经发育障碍，其特征为社交沟通缺陷和重复行为。肠道微生物群在自闭症谱系障碍的病因学中起关键作用，对其进行调节是缓解自闭症样行为的一种有前景的治疗策略。本研究的目的是评估油（ASO）对自闭症小鼠模型BTBR T Itpr3/J（BTBR）小鼠自闭症样行为的影响，并评估相关分子机制。对幼年BTBR小鼠连续36天经口灌胃给予ASO。行为测试表明，ASO显著缓解了BTBR小鼠的自闭症样行为。此外，补充ASO促进了少突胶质细胞的成熟，抑制了小胶质细胞的过度激活，并降低了BTBR小鼠海马中IL-1β和TNF-α的水平。口服ASO还通过降低有害细菌的丰度以及与的比例改善了BTBR小鼠的肠道微生物群失衡。此外，ASO降低了肠道中TNF-α和IL-1β的表达，并增加了ZO-1、claudin-1和occludin的水平，从而减轻肠道炎症并修复肠道屏障损伤。我们的结果表明，ASO在自闭症治疗中具有巨大潜力，为自闭症药物的开发提供了理论依据。
