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.
Keywords: Fas/FasL signaling pathway; M1/M2 polarization of microglia; Traumatic brain injury; β-Asarone.
© 2024. The Author(s) under exclusive licence to Japan Human Cell Society.