To investigate the effects of Tafa2 on microglial functional phenotypes, neuronal injury,
and functional recovery following acute cerebral ischemia. Methods: Transient middle cerebral artery occlusion
(tMCAO) models were established in adult male wild-type mice. The spatiotemporal expression pattern of Tafa2
protein after cerebral ischemia was determined using immunofluorescence techniques. tMCAO models were
established in adult male wild-type and Tafa2-knockout mice. The effects of Tafa2 deletion on microglial
polarization, neuronal apoptosis, and neurological function during the acute phase of cerebral ischemia were
assessed using immunofluorescence, Nissl staining, TUNEL staining, and behavioral tests. Results: In
wild-type mice, Tafa2 protein expression was significantly increased in the ischemic hemisphere on day 3 after
tMCAO compared to that in the sham group. On day 3 after tMCAO, Tafa2-knockout mice exhibited reduced
infarct volume, decreased neuronal apoptosis, and alleviated sensorimotor deficits compared to wild-type mice. 3
days after tMCAO, Tafa2-knockout mice showed an increased proportion of CD206 + microglia and enhanced
phagocytic function compared to wild-type mice. Conclusion: Tafa2 deficiency promotes the polarization of
microglia toward an anti-inflammatory and pro-repair phenotype, reduces neuronal damage and improves
neurological function during the acute phase of ischemic stroke.
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