Yu Ling, Fan Shu-Juan, Liu Li, Xiao Mi, Lin Xiao-Jie, Liu Yong, Lv Hai-Xia, Chen Xin-Lin, Liu Jian-Xin
Department of Neonatology, First Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, 710061, China.
World J Pediatr. 2015 May;11(2):165-70. doi: 10.1007/s12519-014-0519-4. Epub 2014 Nov 20.
A rat model for neonatal hypoxic-ischemic brain damage (HIBD) was established to observe the effect of ischemic postconditioning (IPostC) on cerebral edema and the AQP4 expression following HIBD and to verify the neuroprotection of IPostC and the relationship between changes of AQP4 expression and cerebral edema.
Water content was measured with dry-wet method, and AQP4 transcription and the protein expression of the lesions were detected with real-time PCR and immunohistochemistry staining, respectively.
Within 6-48 hours, the degree of ipsilateral cerebral edema was significantly lower in IPostC-15 s/15 s group than in HIBD group. Similar to the HIBD group, the AQP4 transcription and expression in the IPostC group showed a downward and then upward trend. But the expression was still more evident in the HIBD group than in the IPostC-15 s/15 s group. From 24 to 48 hours, IPostC-15 s/15 s decreased the slowing down expression of AQP4.
IPostC has neuroprotective effect on neonatal rats with HIBD and it may relieve cerebral edema by regulating the expression of AQP4.
建立新生大鼠缺氧缺血性脑损伤(HIBD)模型,观察缺血后处理(IPostC)对HIBD后脑水肿及水通道蛋白4(AQP4)表达的影响,验证IPostC的神经保护作用及AQP4表达变化与脑水肿的关系。
采用干湿法测量含水量,分别用实时荧光定量PCR和免疫组织化学染色检测损伤部位AQP4的转录及蛋白表达。
在6 - 48小时内,IPostC-15 s/15 s组同侧脑水肿程度明显低于HIBD组。与HIBD组相似,IPostC组AQP4转录和表达呈先下降后上升趋势。但HIBD组表达仍比IPostC-15 s/15 s组更明显。在24至48小时,IPostC-15 s/15 s降低了AQP4的延迟表达。
IPostC对新生HIBD大鼠具有神经保护作用,可能通过调节AQP4表达减轻脑水肿。