Tafa2缺失促进脑缺血后小胶质细胞向抗炎表型转化、减轻神经损伤与功能障碍OA

Objective: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.