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目的探讨促红细胞生成素(rhEPO)的神经保护机制。方法新生7日龄Sprague-Dawley(SD)大鼠72只,随机分为3组:假手术组(24只)、缺氧缺血模型组(24只)、rhEPO治疗组(24只),采用Rice方法建立新生大鼠缺氧缺血性脑损伤(HIBD)模型,rhEPO治疗组于缺氧缺血完成后即刻腹腔内注射rhEPO3000U/kg1次,缺氧缺血组则于腹腔内注射等量的生理盐水。各组分别于手术后6、24、48、72h取脑组织切片,用末端脱氧核苷酸转移酶缺口标记法(TUNEL)检测神经细胞凋亡、免疫组织化学方法检测核因子-κB(NF-κB)的表达。结果与假手术组相比缺氧缺血组凋亡细胞数及NF-κB表达随时间的变化增加显著(P<0.05),rhEPO治疗组凋亡细胞数及NF-κB表达随时间的变化下降显著(P<0.05),rhEPO治疗组凋亡细胞数的减少及NF-κB表达减弱呈直线相关(P<0.05)。结论rhEPO对HIBD后海马区神经细胞具有保护作用,其作用机制可能与抑制NF-κB在海马区的持续活化有关。
Objective To investigate the neuroprotective mechanism of erythropoietin (rhEPO). Methods 72 newborn Sprague-Dawley (SD) rats aged 7 days were randomly divided into three groups: sham operation group (24), hypoxic-ischemic model group (24), rhEPO treatment group (24) Rice Hypoxia-Ischemia Brain Damage (HIBD) model was established in neonatal rats. RhEPO-treated mice were intraperitoneally injected rhEPO 3000 U / kg once immediately after hypoxic-ischemic insult and hypoxic-ischemic rats were injected intraperitoneally Physiological saline. The brain tissue sections were taken at 6, 24, 48 and 72 h after operation, and neuronal apoptosis was detected by terminal deoxynucleotidyl transferase nick end labeling (TUNEL). The expressions of nuclear factor-kappa B (NF- κB) expression. Results Compared with the sham operation group, the number of apoptotic cells and the expression of NF-κB in hypoxia-ischemia group increased significantly with time (P <0.05). The number of apoptotic cells and the expression of NF-κB in rhEPO-treated group decreased with time (P <0.05). The number of apoptotic cells and the decrease of NF-κB in rhEPO treatment group were linearly correlated (P <0.05). Conclusions rhEPO can protect neurons in hippocampus after HIBD, and its mechanism may be related to the inhibition of sustained activation of NF-κB in hippocampus.