目的　研究新生大鼠缺氧缺血性脑病 (HIE)时脑组织单核细胞趋化蛋白 - 1(MCP - 1)的表达及地塞米松对其影响。方法　 2 5只新生大鼠分为 3组 :HIE模型对照组 (对照组 ) ,大剂量地塞米松治疗组 (大剂量组 ) ,小剂量地塞米松治疗组 (小剂量组 ) ;于造模后腹腔内分别注射生理盐水 10ml/kg ,地塞米松 10mg/kg及地塞米松 0 .5mg/kg ;2 4h后处死后取脑组织 ,免疫组化法检查脑组织MCP - 1蛋白的表达 ,光镜检查脑病理改变情况。结果　对照组、大剂量组、小剂量组的MCP - 1蛋白 ,神经细胞总数及变性 /坏死神经细胞数 ,分别为 7.98±1.37% ,0 .97± 0 .42 % ,7.2 5± 2 .45 % ;15 8.0 7± 14.48个 / 6HP ,2 0 3.2 5± 10 .2 7个 / 6HP ,15 5 .11± 16 .6 1个 / 6HP ,2 2 .86± 3.13个 / 6HP ,17.75± 3.45个 / 6HP ,2 3.89± 4.18个 / 6HP。与对照组相比 ,大剂量组MCP - 1蛋白表达减少 (P <0 .0 1) ,神经细胞总数增加 (P <0 .0 5 )及变性 /坏死神经细胞数减少 (P <0 .0 1) ,而小剂量组改变不明显(P >0 .0 5 )。结论　大剂量地塞米松可能通过降低HIE脑组织中MCP - 1蛋白表达对HIE脑组织损伤产生保护作用。 Objective To investigate the expression of monocyte chemoattractant protein - 1 (MCP - 1) in neonatal rats with hypoxic - ischemic encephalopathy (HIE) and the effect of dexamethasone on it. Methods 25 neonatal rats were divided into three groups: HIE model control group (control group), high-dose dexamethasone treatment group (high-dose group) and low-dose dexamethasone treatment group (low dose group) After intraperitoneal injection of normal saline 10ml / kg, dexamethasone 10mg / kg and dexamethasone 0.5mg / kg; 2 4h after sacrifice, brain tissue was taken out and the expression of MCP - 1 protein in brain tissue was examined by immunohistochemistry. Light microscope to check the pathological changes of the brain. Results The number of MCP - 1 protein, the total number of neurons and the number of degenerative / necrotic neurons in the control group, high dose group and low dose group were 7.98 ± 1.37%, 0.97 ± 0.42%, 7.25 ± 2.45 %; 15 8.0 7 ± 14.48 / 6HP, 20 3.2 5 ± 10.27 / 6HP, 15 5 .11 ± 16.61 / 6HP, 22.6 ± 3.13 / 6HP, 17.75 ± 3.45 / 6HP, 2 3.89 ± 4.18 / 6HP. Compared with the control group, the MCP - 1 protein expression in high dose group decreased (P <0.01), the total number of nerve cells increased (P <0.05) and the number of degeneration / necrosis neurons decreased (P <0. 0 1), while the small dose group did not change significantly (P> 0.05). Conclusion High - dose dexamethasone may protect the brain tissue from HIE injury by decreasing the expression of MCP - 1 protein in HIE brain tissue.