Xiong Yue, Chen Jianhui, Lv Mingqi, Wang Feifei, Zhang Hanhong, Tang Boyi, Li Yingbo
Cerebrovascular Diseases Laboratory, Institute of Neuroscience, Chongqing Medical University, Chongqing 400016, China.
Experimental Teaching Management Center of Chongqing Medical University, Chongqing 400016, China.
Int Immunopharmacol. 2023 Apr;117:109885. doi: 10.1016/j.intimp.2023.109885. Epub 2023 Feb 27.
Inflammation plays an essential role in the pathogenesis of autism spectrum disorder (ASD). Thymol is a bioactive monoterpene isolated from Thymus vulgaris that has anti-inflammatory properties and is helpful in neurodevelopmental disorders. The purpose of this study was to investigate the effects of thymol on autism-like behaviours in rats with VPA-induced ASD and to assess the related molecular mechanisms. In the prefrontal cortex (PFC) of the valproic acid (VPA)-exposed rat model, the levels of Pin1, phosphorylated p38 MAPK, interleukin-1β (IL-1β) and tumour necrosis factor (TNF)-α, were increased, and the levels of PSD95 and synaptophysin (SYP) decreased. After thymol treatment (30 mg/kg), the VPA-induced autism-like behaviours were alleviated. Moreover, thymol also rescued the dysregulated levels of Pin1, phosphorylated p38 MAPK, IL-1β, TNF-α, PSD95, and SYP. In addition, immunofluorescence experiments showed that thymol treatment decreased the correlation between Pin1 and phosphorylated p38 MAPK. Mechanistically, Pin1 knockdown by RNA interference confirmed that Pin1 promotes inflammation via phosphorylation of p38 MAPK in the VPA exposure rat model. In conclusion, thymol improved autism-like behaviours in VPA-induced ASD rats by reducing inflammation and improving neurodevelopment. This effect was mediated by the Pin1/p38 MAPK pathway. These results experimentally provide the potential for thymol in new therapeutic avenues for autism.
炎症在自闭症谱系障碍(ASD)的发病机制中起着至关重要的作用。百里香酚是一种从百里香中分离出的具有生物活性的单萜,具有抗炎特性,有助于治疗神经发育障碍。本研究的目的是探讨百里香酚对丙戊酸(VPA)诱导的ASD大鼠自闭症样行为的影响,并评估相关的分子机制。在暴露于丙戊酸(VPA)的大鼠模型的前额叶皮质(PFC)中,Pin1、磷酸化p38丝裂原活化蛋白激酶(MAPK)、白细胞介素-1β(IL-1β)和肿瘤坏死因子(TNF)-α的水平升高,而突触后密度蛋白95(PSD95)和突触素(SYP)的水平降低。百里香酚治疗(30mg/kg)后,VPA诱导的自闭症样行为得到缓解。此外,百里香酚还挽救了Pin1、磷酸化p38 MAPK、IL-1β、TNF-α、PSD95和SYP的失调水平。此外,免疫荧光实验表明,百里香酚治疗降低了Pin1与磷酸化p38 MAPK之间的相关性。机制上,通过RNA干扰敲低Pin1证实,在VPA暴露的大鼠模型中,Pin1通过p38 MAPK的磷酸化促进炎症。总之,百里香酚通过减轻炎症和改善神经发育,改善了VPA诱导的ASD大鼠的自闭症样行为。这种作用是由Pin1/p38 MAPK途径介导的。这些结果通过实验为百里香酚在自闭症新治疗途径中的应用提供了可能性。