目的：探究急性脑缺血后Tafa2对小胶质细胞功能表型及脑缺血后神经损伤与功能重建的影响。方
法：构建成年雄性野生型小鼠短暂性大脑中动脉梗死（transient middle cerebral artery occlusion，tMCAO）模
型，采用免疫荧光技术明确Tafa2蛋白在脑缺血后的时空表达特征。构建成年雄性野生型及Tafa2敲除小鼠
的tMCAO模型，通过免疫荧光、尼氏染色、TUNEL染色及行为学测定等方法，探究敲除Tafa2对脑缺血急性
期的小胶质细胞表型转化、神经元凋亡以及小鼠神经功能的影响。结果：在野生型小鼠中，与假手术组相
比，tMCAO后3 d小鼠缺血侧脑组织中的Tafa2蛋白表达量明显增高。tMCAO术后3 d，与野生型小鼠相
比，Tafa2敲除小鼠中梗死面积减小，神经元凋亡减少，感觉与运动功能缺陷缓解。tMCAO术后3 d，与野生
型小鼠相比，Tafa2敲除小鼠中CD206+
的小胶质细胞比例增加，吞噬功能增强。结论：脑缺血梗死后急性
期，Tafa2缺失可促进小胶质细胞向抗炎促修复表型转化，减轻神经损伤，改善神经功能。
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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