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马玉姗, 周俊, 柳慧, 等. rhEPO预处理对胎鼠宫内缺血缺氧性脑损伤的保护作用及Caspase-3表达的影响[J]. koko体育app 学报（医学版）, 2013, 44(3): 397-401.
引用本文: 马玉姗, 周俊, 柳慧, 等. rhEPO预除理对胎鼠宫腔内脑供血不足异星工厂性脑板材损害的保护英文目的及Caspase-3传达的影晌[J]. 湖北大专学报（医药学版）, 2013, 44(3): 397-401.
MA Yu-shan, ZHOU Jun, LIU Hui, et al. Protection Effect of Recombiant Human Erythropoietin Preconditioning Against Intrauterine Hypoxic-ischemic Brain Injury and its Influence on Expression of Caspase-3 Protein in Brain Tissue[J]. Journal of Sichuan University (Medical Sciences), 2013, 44(3): 397-401.
Citation: MA Yu-shan, ZHOU Jun, LIU Hui, et al. Protection Effect of Recombiant Human Erythropoietin Preconditioning Against Intrauterine Hypoxic-ischemic Brain Injury and its Influence on Expression of Caspase-3 Protein in Brain Tissue[J]. Journal of Sichuan University (Medical Sciences), 2013, 44(3): 397-401.

rhEPO预处理对胎鼠宫内缺血缺氧性脑损伤的保护作用及Caspase-3表达的影响

Protection Effect of Recombiant Human Erythropoietin Preconditioning Against Intrauterine Hypoxic-ischemic Brain Injury and its Influence on Expression of Caspase-3 Protein in Brain Tissue

  • 摘要: 目的 探讨重组人促红细胞生成素(rhEPO)对胎鼠宫内缺血缺氧性脑损伤后神经细胞凋亡及Caspase-3蛋白表达的影响。 方法 将44只孕19 d SD大鼠分为rhEPO治疗组(Treat组)、生理盐水缺血对照组(I/R组)和假手术对照组(Sham组)。Treat组于缺血缺氧前30 min经尾静脉注入rhEPO (5000 U/kg),I/R组于缺血缺氧前30 min注入1 mL生理盐水。各组分别于缺血再灌注后30 min、3 h、6 h、24 h和48 h取胎鼠脑组织。假手术对照组经尾静脉注入1 mL生理盐水后只进行开关腹手术,于术后24 h取胎鼠脑组织。采用免疫组化方法检测活化的Caspase-3蛋白的表达,并通过末端脱氧核苷酸转移酶缺口标记(Tunel)法观察脑神经元凋亡情况。 结果 I/R组与Treat组缺血再灌注24 h和48 h海马区均观察到凋亡的脑神经细胞存在,且凋亡神经元的数量随再灌注时间的延长而增加。Treat组与I/R组比较,Tunel阳性细胞数减少,在再灌注48 h时,差异有统计学意义(P<0.01)。I/R组Caspase-3蛋白表达阳性强度随再灌注时间的延长逐渐增加,在再灌注48 h时最高。与I/R组相比较,Treat组Caspase-3蛋白表达减弱, Caspase-3表达的面积积分光密度值减小,除24 h外其余各时间点比较差异均有统计学意义(P<0.01)。 结论 rhEPO预处理可抑制胎鼠宫内缺血缺氧后脑组织中Caspase-3蛋白的表达以及神经细胞的凋亡,对缺血缺氧性脑损伤具有一定的保护作用。  
    Abstract: Objecitve To investigate the effects of recombine human erythropoietin (rhEPO) on neural cells apoptosis and the expression of Caspase-3 protein in brain tissue of fetal rats after intrauterine hypoxic-ischemic brain injury. Methods Forty-four Sprague-Dawley rats on 19 days of pregnancy were divided into rhEPO treated group, ischemia-reperfusion group and sham-operated group. Intrauterine hypoxic-ischemic injury of fetal rats was induced by bilateral occlusion of the utero-ovarian artery for 20 min. rhEPO (5000 U/kg) was injected into rats through caudal vein in rhEPO treated group while saline was injected into rats in hypoxic-ischemic group 30 min before hypoxic-ischemic injury. The brain samples in rhEPO treated group and hypoxic-ischemic group were obtained at 30 min,3 h,6 h,24 h and 48 h respectively after artery clamping. There was no hypoxic-ischemic injury in sham-operated group, so the brain samples were obtained at 24 hours after sham operation. Neuroapoptosis in brain tissue was measured by TdT mediated dUTP-biotin nick end labeling (Tunel) staining. The expression of Caspase-3 protein was observed by immunohistochemistry. Results The number of apoptosis cells in fetal rat hippocampus after intrauterine hypoxic-ischemic increased progressively with reperfusion. Compared with the I/R group, the number of apoptosis cells decreased in rhEPO treated group (P<0.01). The expression of Caspase-3 increased rapidly after 3 hours from the reperfusion in the I/R group. Compared with the I/R group, there was less expression of Caspase-3 in rhEPO treated group (P<0.01). Conclusion rhEPO showed the effects to inhibit the apoptosis of fetal neural cells and the expression of Caspase-3 protein due to intrauterine hypoxic-ischemic brain injury.  
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