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目的建立孕兔宫内窘迫模型,探讨硫酸镁(MgSO4)胎兔脑损伤后NMDAr1表达的影响。方法新西兰大白兔孕兔39只,随机分为空白对照组(n=12)、假手术组(n=9)、缺血缺氧脑病组(n=9)和MgSO4保护组(n=9),缺血缺氧组和MgSO4保护组建立孕兔开腹子宫动脉结扎胎兔宫内窘迫缺血缺氧模型,并且MgSO4保护组在建立模型前给予腹腔注射MgSO4(100 mg/kg),分别开腹取各组胎兔脑组织做病理及NMDAr1表达检测。结果与空白对照组和假手术比较,缺血缺氧脑病组和MgSO4保护组NMDAr1表达强阳性,脑组织结构层次被破坏,神经细胞变性坏死,间质出血;MgSO4保护组NMDAr1免疫反应强度低于缺血缺氧脑病组,而脑组织结构层次完整性优于缺血缺氧脑病组。结论 MgSO4在一定程度上能减轻NMDAr1导致的胎儿宫内窘迫缺血缺氧病理性脑损伤,对NMDA脑损伤具有一定的保护作用。
Objective To establish a model of intrauterine distress in pregnant rabbits to investigate the effect of magnesium sulfate on the expression of NMDAr1 after brain injury in rabbits. Methods Thirty-nine New Zealand white rabbits were randomly divided into blank control group (n = 12), sham operation group (n = 9), ischemia hypoxic encephalopathy group (n = 9) and MgSO4 protection group , Ischemia / hypoxia group and MgSO4 protection group. The model of ischemia / reperfusion in rabbits with intrauterine fetal distress was established by ligating the uterine artery of rabbits with laparotomy. The rats in MgSO4 group were intraperitoneally injected with MgSO4 (100 mg / kg) Taken abdomen from each group to make pathological and fetal brain tissue NMDAr1 expression. Results Compared with the blank control group and the sham operation group, the expression of NMDAr1 in hypoxic-ischemic encephalopathy group and MgSO4-protected group was strongly positive, and the structure of brain tissue was destroyed. The degeneration and necrosis of nerve cells and interstitial hemorrhage were also observed. The intensity of NMDAr1 immunoreactivity in MgSO4- Hypoxic-ischemic encephalopathy group, while the level of brain tissue structure integrity better than ischemic hypoxic-encephalopathy group. Conclusion MgSO4 can alleviate the ischemic and hypoxic-ischemic brain damage induced by NMDAr1 to a certain extent, and protects the brain from NMDA injury.