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. 2024 Dec 24;38(1):33.
doi: 10.1007/s13577-024-01161-z.

β-Asarone regulates microglia polarization to alleviate TBI-induced nerve damage via Fas/FasL signaling axis

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β-Asarone regulates microglia polarization to alleviate TBI-induced nerve damage via Fas/FasL signaling axis

Mingyue Xia et al. Hum Cell. .

Abstract

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.

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Conflict of interest statement

Declarations. Conflict of interest: The authors have no conflict of interest. Ethical approval: The protocols were conformed to the Animal Research: Reporting In Vivo Experiments Guidelines and approved by the Institutional Animal Care and Use Committee, Xiangya Hospital, Central South University (No. 202310196).

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