Xia Mingyue, Yi Min, Guo Chunyuan, Xie Yeli, Yu Wenting, Wang Dongsheng, Dai Xingping
Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Jiangxi Hospital, National Reginal Center for Neurological Disease, Honggutan District, No.266 Fenghe North Avenue, Nanchang, 330038, Jiangxi, China.
National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Hum Cell. 2024 Dec 24;38(1):33. doi: 10.1007/s13577-024-01161-z.
Acute injury and secondary injury caused by traumatic brain injury (TBI) seriously threaten the health of patients. The purpose of this study was to investigate the role of β-Asarone in TBI-induced neuroinflammation and injury. In this work, the effects of β-Asarone on nerve injury and neuronal apoptosis were investigated in mice with TBI by controlled cortical impingement. The results of this research implied that β-Asarone dose-dependently decreased the mNSS score, brain water content and neuronal apoptosis, but increased the levels of the axonal markers Nrp-1 and Tau in TBI mice. In addition, β-Asarone caused a decrease in the levels of Fas, FasL, and inflammatory factors in cerebrospinal fluid and serum of TBI mice. Therefore, β-Asarone inhibited neuroinflammation and promoted axon regeneration in TBI mice. Besides, β-Asarone treatment inhibited M1 phenotype polarization but promoted M2 phenotype polarization in microglia of TBI mice. Overexpression of Fas and FasL reversed the above effects of β-Asarone. Thus, β-Asarone regulated microglial M1/M2 polarization balance in TBI mice by suppressing Fas/FasL signaling axis. In conclusion, β-Asarone inhibited Fas/FasL signaling pathway to promote the M1/M2 polarization balance of microglia toward M2 polarization, thus alleviating TBI-induced nerve injury.
创伤性脑损伤（TBI）所致的急性损伤和继发性损伤严重威胁患者健康。本研究旨在探讨β-细辛醚在TBI诱导的神经炎症和损伤中的作用。在本研究中，通过控制性皮质撞击法，研究β-细辛醚对TBI小鼠神经损伤和神经元凋亡的影响。本研究结果表明，β-细辛醚剂量依赖性地降低了TBI小鼠的mNSS评分、脑含水量和神经元凋亡，但增加了轴突标记物Nrp-1和Tau的水平。此外，β-细辛醚使TBI小鼠脑脊液和血清中Fas、FasL及炎症因子水平降低。因此，β-细辛醚可抑制TBI小鼠的神经炎症并促进轴突再生。此外，β-细辛醚处理可抑制TBI小鼠小胶质细胞的M1表型极化，但促进M2表型极化。Fas和FasL的过表达逆转了β-细辛醚的上述作用。因此，β-细辛醚通过抑制Fas/FasL信号轴调节TBI小鼠小胶质细胞的M1/M2极化平衡。综上所述，β-细辛醚抑制Fas/FasL信号通路，促进小胶质细胞的M1/M2极化平衡向M2极化方向转变，从而减轻TBI诱导的神经损伤。
