不同剂量重组人促红细胞生成素在宫内缺血缺氧环境中透过胎盘屏障及血脑屏障的通透性
Erythropoietin through the Placenta Barrier and Fetal Blood-Brain Barrier with Transient Uteroplacental Ischemia
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摘要: 目的 探讨不同剂量重组人促红细胞生成素(recombinant human erythropoietin,rhEPO)在宫内缺血缺氧时透过胎盘屏障及胎鼠血脑屏障的通透性。 方法 孕19 d(孕晚期)SD大鼠,分为3组:rhEPO治疗组(Treat组)、假手术对照组(Sham组)和生理盐水缺血对照组(I/R组)。Treat组和I/R组制备宫内缺血缺氧模型,Sham组只进行开关腹手术。Treat组和Sham组根据注射rhEPO的剂量不同各自再分为3组,分别在宫内缺血缺氧处理或开关腹手术前30 min经孕鼠尾静脉注射125I标记的rhEPO 2500 U/kg、5000 U/kg、7500 U/kg,I/R组在宫内缺血缺氧处理前30 min经尾静脉注入生理盐水。均于缺血缺氧处理或开关腹手术后24 h取胎盘、羊水及胎鼠脑、肝、心、肺和肾,检测并比较各组织中125I-rhEPO的放射比活性。 结果 Treat组和Sham组胎盘、羊水及胎鼠各组织中均能检测到125I-rhEPO的分布。125I-rhEPO在胎盘、羊水及胎鼠各组织中的分布均随rhEPO注射剂量的增加而增加。在各剂量组中,Treat组胎鼠各组织中的125I-rhEPO含量均高于Sham组(P<0.05)。 结论 在宫内缺血缺氧环境下,胎盘屏障及胎鼠血脑屏障对外源性rhEPO的通透性增加。Abstract: Objective To observe the permeability of recombinant human erythropoietin through placenta barrier and fetal blood-brain barrier after transient uteroplacental ischemia. Methods Rats on days 19 of pregnancy were divided into rhEPO treated group, ischemia-reperfusion group and sham-operated group. Fetal ischemia in rhEPO treated group and ischemia-reperfusion group was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. Different dosage of 125I-rhEPO (2500 U/kg,5000 U/kg,7500 U/kg) was injected into the rats through caudal veins 30 min before injury in rhEPO treated group and sham-operated group. Saline was administered intravenously 30 min before the induction of hypoxic-ischemic injury in ischemia-reperfusion group. The amniotic fluid, placenta and fetal organs including brain, liver, heart, lung and kidney were collected to measure the radioactivity at 24h after injury. Results 125I-rhEPO was detected in amniotic fluid, placenta and fetal organs. The radioactivity of 125I-rhEPO in these tissues increased gradually with the increased dose injected in rhEPO treated group and sham-operated group. There were significant differences in the radioactivity of 125I-rhEPO between rhEPO treated group and sham-operated group (P<0.05). Conclusion The permeability of rhEPO through placental barrier and blood-brain barrier increased under the condition of fetal ischemia and hypoxia.
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