目的:探讨人脐带血间充质干细胞(mesenchymal stem cells,MSC)移植对脑梗死大鼠外周血Foxp3调节性T细胞改善缺血性脑损害的可能机制。方法选择SD大鼠40只,随机分为假手术组、对照组、生理盐水组、MSC组,每组10只。各组大鼠分别测定1 d、7 d、14 d、28 d外周血单个核细胞中Foxp3 mRNA表达和神经功能缺损评分;TUNEL法检测神经细胞凋亡数。结果 MSC组14 d、28 d神经功能缺损评分明显低于对照组及生理盐水组[(6.1±1.4)分vs (7.3±1.1)分,(7.3±0.9)分;(5.2±1.0)分vs (6.2±1.0)分,(6.3±0.5)分;P<0.05];28 d凋亡细胞数明显少于对照组及生理盐水组(P<0.05)。对照组、生理盐水组及MSC组1 d、7 d、14 d、28 d外周血Foxp3 mRNA表达明显高于假手术组,差异有统计学意义(P<0.01)。MSC组1 d、7 d外周血Foxp3 mRNA表达明显高于对照组和生理盐水组,差异有统计学意义(P<0.05)。结论 MSC移植改善大鼠急性脑缺血神经功能恢复的机制之一,可能与上调免疫炎性反应初期Foxp3 mRNA表达有关。
Objective To explore the possible mechanisms of human umbilical cord blood mesenchymal stem cells(hUCB-MSCs) transplantation on improving ischemic brain damage ,Foxp3 expression in peripheral blood was observed inrats following focal cerebral ischemia reperfusion (I/R).Methods 40 healthy SD rats were randomly divided into shamoperation group,I/R group,saline group and hUCB-MSCs group.Foxp3 mRNA expression in peripheral blood mononuclearcells and modified neurological severity score (mNSS) were measured 1 d,7 d,14 d and 28 d after reperfusion.Neural cellapoptosis was detected by TUNEL 4 w after reperfusion.Results mNSS in hUCB-MSCs group 14 d and 28 d after reperfusionwas significantly lower than that of control group and saline group [(6.1 ±1.4) points vs (7.3 ±1.1) points,(7.3 ±0.9) points;(5.2 ±1.0) points vs (6.2 ±1.0) points,(6.3 ±0.5) points;P 〈0.05].The number of neural cell apoptosisin hUCB-MSCs was obviously less than that of control group and saline group 28 d after reperfusion (P 〈0.05).Foxp3mRNA expression level in hUCB-MSCs group was significantly higher than that of control group and saline group 1 d and7 d after reperfusion (P 〈0.05).Conclusion Up-regulation of Foxp3 mRNA expression is one of the possible mechanismsof hUCB-MSCs transplantation on improving ischemic brain damage the mechanisms of inhibiting inflammatory reac -tion.