【摘要】 目的：探索γδT细胞受体对心脏骤停-心肺复苏（CPCR）后脑缺血再灌注小鼠体内Treg及相关细胞因子的影响。方法：90只雄性C57BL/6小鼠随机分为CPCR组、对照组和CPCR+γδT细胞受体拮抗组（CPCR后注射γδT细胞受体拮抗剂），每组30只。收集小鼠脑组织，TUNEL检测神经元凋亡，HE染色观察神经元损伤情况，Western blot检测脑组织Foxp3蛋白表达，ELISA检测血清中MPO活性、TNF-α、IL-6和IL-1β浓度。结果：与对照组相比，CPCR组小鼠神经元凋亡显著增加（P<0.05），脑组织损伤严重，MPO活性、TNF-α、IL-6和IL-1β浓度显著上升（P<0.05）,Foxp3表达显著下调。与CPCR组相比，CPCR+γδT细胞受体拮抗组大鼠神经元凋亡减少（P<0.05），脑组织损伤减轻，MPO活性、TNF-α、IL-6和IL-1β浓度明显降低（P<0.05）,Foxp3表达显著上调。结论：γδT细胞受体拮抗剂可通过抑制炎症反应缓解CPCR后脑缺血再灌注损伤。更多还原

【Abstract】 Objective:To explore effects of γδT cell receptor on Treg and related cytokines in mice with cerebral ischemiareperfusion after cardiac arrest cardiopulmonary resuscitation(CPCR).Methods:Ninety male C57BL/6 mice were randomly divided into CPCR group,control group and CPCR+γδT cell receptor antagonist group(γδT cell receptor antagonist injection after CPCR),with 30 mice in each group. Brain tissues were collected. TUNEL was used to detect neuronal apoptosis;HE staining was used to observe damage of neurons;Western blot was used to detect expression of Foxp3 protein in brain tissue;ELISA was used to detect serum MPO activity and concentrations of TNF-α,IL-6 and IL-1β.Results:Compared with control group,neuron apoptosis of mice in CPCR group was significantly increased(P<0.05),brain tissue damage was significantly increased,activity of MPO and concentrations of TNF-α,IL-6,IL-1β were increased significantly(P<0.05),Foxp3 expression was decreased significantly. Compared with CPCR group,neuron apoptosis of mice in CPCR+γδT cell receptor antagonist group was reduced(P<0.05),brain tissue damage was significantly reduced,MPO activity,concentrations of TNF-α,IL-6 and IL-1β were decreased significantly(P<0.05),and expression of Foxp3 was increased significantly(P<0.05).Conclusion:γδT cell receptor antagonists can improve cerebral ischemia-reperfusion injury after CPCR by inhibiting inflammatory reaction.更多还原