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目的 研究骨髓单个核细胞(BMMNCs)对脑梗死小鼠神经元变性死亡的影响.方法 将雄性昆明小鼠随机分为PBS治疗组和BMMCs治疗组.线栓法制作小鼠大脑中动脉栓塞(MCAO)模型;梯度离心法提取BMMNCs;酶联免疫吸附法(ELISA)评价常氧及低氧培养条件下BMMNCs分泌IL-10、VEGF和IGF-1的能力.脑梗死后6h经尾静脉注射BMMNCs或PBS,脑梗后1,4,7d采用神经功能损害评分表(mNSS)、免疫荧光法、Fluoro-Jade B(FJB)染色进行神经功能、小胶质细胞活性及神经元变性死亡数目的评估.脑梗死后7d,TTC染色评价脑梗死体积.结果 (1)BMMNCs在常氧或低氧条件下培养24h后,低氧环境下BMMNCs分泌细胞因子(IL-10、VEGF和IGF-1)的能力明显强于常氧环境,差异有统计学意义(P＜0.05);(2)与PBS治疗组相比,BMMNCs治疗组小鼠在脑梗死后第4,7天的mNSS评分、小胶质细胞的活性、神经元变性死亡数量均显著降低,差异有统计学意义(P＜0.05);(3) BMMNCs治疗组小鼠脑梗死体积[(27.8±7.5)％]明显小于PBS治疗组[(37.1±6.9)％],差异有统计学意义(P＜0.05).结论 骨髓单个核细胞可通过分泌细胞因子IL-10、VEGF和IGF-1抑制小胶质细胞的活性,明显抑制脑梗死后神经元的变性死亡,减少脑梗死体积,促进神经功能恢复.“,”Objective To investigate the effects of bone marrow mononuclear cells (BMMNCs) on neurodegeneration after cerebral ischemia in mice.Methods Adult male mice were randomly divided into PBS treated group and BMMNCs treated group.The model was established with suture emboli method;BMMNCs were isolated with density gradient centrifugation method.The production of cytokines from BMMNCs including interleukin-10 (IL-10),vascular endothelial growth factor (VEGF) and insulinlike growth factor-Ⅰ (IGF-1) were tested by enzyme-linked immunosorbent assay (ELISA) under normoxic or hypoxic conditions.Mice were injected with PBS or BMMNCs via tail vein 6 h after ischemia reperfusion.Neurological functional deficits,the activity of microglial cell and neurodegenration were assessed on day 1,4,7 after MCAO,and infarct volume was assessed on day 7.Results (1) Compared with BMMNCs under normoxic conditions,BMMNCs under hypoxic conditions secreted more IL-10,VEGF,IGF-1 after 24h of cultivation(P＜0.05).(2) BMMNCs transplantation significantly reduced neurologic functional deficits and the number of activated microglia and degenerated neurons on days 4,7 compared with PBS treated groups (P＜0.05).(3) Compared with PBS treated group ((37.1 ± 6.9) ％),BMMNCs transplantation significantly reduced infarct volume((27.8±7.5)％) (P＜0.05).Conclusion Bone marrow mononuclear cells can significantly inhibit neurodegeneration,promote neurological recover and reduce infarct volume through inhibition of microglial cell activation by secretion of cytokines including IL-10,VEGF and IGF-1.