Park Jee Yoon, Byeon Jung Hye, Park Sung-Won, Eun So-Hee, Chae Kyu Young, Eun Baik-Lin
Department of Pediatrics, Korea University, College of Medicine, 126-1 Anam-Dong, Sungbuk-Gu, Seoul, Republic of Korea.
Brain Dev. 2013 Jan;35(1):68-74. doi: 10.1016/j.braindev.2012.01.009. Epub 2012 Feb 13.
We investigated the neuroprotective effects of human placental extracts (HPE) and the effects of HPE on recovery of cognitive and behavioral function on hypoxic-ischemic brain injury in the newborn rat. The right common carotid arteries of 7-day-old rats were coagulated, and rats were then exposed to 8% oxygen. Immediately before and again at three times after the hypoxia-ischemia (pre-treatment group), and immediately after and three times again after hypoxia-ischemia (post-treatment group), the rats were intraperitoneally injected with HPE (0.1, 0.25, or 0.5 mL/10 g/dose). No-treatment rats received saline only. On postnatal day 12, brains were removed and gross morphological damage was evaluated. To quantify the severity of brain injury, bilateral cross-sectional areas of the anterior commissural and posterior hippocampal levels were analyzed with NIH Image. Assessments of the open field activity levels at 2, 4, 6 and 8 week and, the Morris water maze test at 8 weeks after hypoxia-ischemia were carried out according to standard methods. HPE pre-treatment decreased the incidence of liquefactive cerebral infarction, at an optimally neuroprotective dose of 0.5 mL/10 g/dose (P<0.05). In the Morris water maze test, the group injected with HPE at 0.5 mL/10 g/dose concentration showed shorter escape latencies than the no-treatment group (P<0.05). These findings support a protective effect of the HPE treatment on neuronal integrity and cognitive function following hypoxic-ischemic brain injury. Injected at an appropriate dose prior to exposure, HPE may significantly reduce or prevent hypoxic-ischemic injury in the immature brain.
我们研究了人胎盘提取物（HPE）的神经保护作用以及HPE对新生大鼠缺氧缺血性脑损伤后认知和行为功能恢复的影响。对7日龄大鼠的右侧颈总动脉进行结扎，然后将大鼠置于8%氧气环境中。在缺氧缺血前即刻以及缺氧缺血后三次（预处理组），以及在缺氧缺血后即刻和三次（后处理组），给大鼠腹腔注射HPE（0.1、0.25或0.5 mL/10 g/剂量）。未处理的大鼠仅接受生理盐水。在出生后第12天，取出大脑并评估大体形态损伤。为了量化脑损伤的严重程度，用NIH Image分析前连合和后海马水平的双侧横截面积。根据标准方法在缺氧缺血后2、4、6和8周进行旷场活动水平评估，并在8周时进行莫里斯水迷宫试验。HPE预处理以0.5 mL/10 g/剂量的最佳神经保护剂量降低了液化性脑梗死的发生率（P<0.05）。在莫里斯水迷宫试验中，以0.5 mL/10 g/剂量浓度注射HPE的组比未处理组的逃避潜伏期更短（P<0.05）。这些发现支持HPE治疗对缺氧缺血性脑损伤后神经元完整性和认知功能的保护作用。在暴露前以适当剂量注射，HPE可能显著减少或预防未成熟脑的缺氧缺血性损伤。
