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Updated: Jul 22, 2025
A Simplified Operation for the Endovascular Perforation Murine Model of Subarachnoid Hemorrhage
Published on: June 13, 2025
CXCR2 antagonism attenuates neuroinflammation after subarachnoid hemorrhage
1Department of Neurosurgery, Chengdu Second People's Hospital, No. 10, Qingyun South Street, Chengdu 610021, Sichuan, China.
Objectives:
Overactivation of neuroinflammation can worsen the prognosis of subarachnoid hemorrhage (SAH) patients. CXCR2 is a widely expressed G protein-coupled receptor that participates in the regulation of inflammation, indicating a potential role of CXCR2 in SAH.
Materials And Methods:
Herein, we examined the expression pattern of CXCR2 in the ipsilateral brain tissue of SAH mice. Then, we evaluated the effects of CXCR2 antagonist on neuroinflammation and neurological function after SAH.
Results:
Western blotting and immunohistochemistry revealed that CXCR2 expression was upregulated following SAH. Our results demonstrated that treatment with SB225002 inhibited inflammatory cytokine (IL-1β, IL-6, TNF-α, MCP-1) production in the brain and cerebrospinal fluid (CSF) following SAH. Our further findings confirmed that treatment with SB225002 ameliorated astrocytosis and microgliosis after SAH. Interestingly, SB225002 significantly improved neurological impairment after SAH.
Conclusions:
Altogether, these results suggest that pharmacologically targeting CXCR2 may be an effective disease-modifying treatment for SAH.
