临床儿科杂志 ›› 2014, Vol. 32 ›› Issue (4): 368-371.

• 实验研究 • 上一篇    下一篇

谷氨酸受体在新生大鼠缺氧缺血脑损伤海马组织中的表达

唐晓娟1, 孙斌1, 王莹1, 丁欣1, 于论1, 徐利晓2, 冯星1   

  1. 苏州大学附属儿童医院1.新生儿科, 2.儿科研究所(江苏苏州 215003)
  • 收稿日期:2013-06-14 出版日期:2014-04-15 发布日期:2014-04-15

The expression of glutamate receptor in hippocampus of neonatal rats with hypoxic-ischemic brain damage 

TANG Xiaojuan1, SUN Bin1, WANG Ying1, DING Xin1, YU Lun1, XU Lixiao2, FENG Xing1    

  1. (1.Department of Neonatology, Children's Hospital Affiliated to Soochow University, Suzhou 215003, Jiangsu, China; 2.Institute of Pediatrics, Children's Hospital Affiliated to Soochow University, Suzhou 215003, Jiangsu, China)
  • Received:2013-06-14 Online:2014-04-15 Published:2014-04-15

摘要:

 目的 探讨Ca-A/K通道相关分子谷氨酸受体1(GluR1)及谷氨酸受体2(GluR2)在新生大鼠缺氧缺血脑损伤(HIBD)后海马组织中表达以及在自噬发生中的作用。方法 选取7日龄SD新生大鼠60只,随机分为HIBD组和假手术组,于HIBD造模后0、1、6、24、48、72 h取海马组织,采用Western blot法检测GluR2、GluR1及自噬标记蛋白LC3、Beclin-1的表达。结果 HIBD组6 h后脑组织即出现水肿,可见点状软化坏死灶。与假手术组相比,各时间点HIBD组的GluR2表达水平均下降,而GluR1、Beclin-1、LC3表达水平均增加,差异有统计学意义(P均<0.05)。HIBD组海马组织中LC3、Beclin-1、GluR1 和GluR2蛋白表达水平在HIBD造模后各个时间点间差异有统计学意义(F=10.65~701.14,P均<0.01)。GluR2蛋白表达于HIBD后1 h即开始下降,6 h下降较明显,24 h达最低点;GluR1、Beclin-1及LC3表达于6 h开始增加,24 h达高峰,48 h仍持续较高水平;上述蛋白表达均在72 h逐渐恢复。结论 Ca-A/K通道相关分子GluR2及GluR1在新生大鼠HIBD后海马组织自噬性死亡中发挥重要的作用。

Abstract:  Objective To study the expression of Ca-A/K channel-related molecules glutamate receptor 2 and 1(GluR2/1) in hippocampus tissues of neonatal rats with hypoxic-ischemic brain damage (HIBD). Methods A total of 60 7-day-old Sprague-Dawley rats were randomly divided into sham operation group and HIBD group. Hippocampal tissues were obtained at 0 h, 1 h, 6 h, 24 h, 48 h and 72 h after HIBD. The expression of GluR2, GluR1 and autophagy marker protein Beclin-1, LC3 were detected by Western blot assay. Results Edema and focal softening and necrosis were observed 6 h after HIBD in the brains of neonatal rats. Compared with Con group, at each time point, the expression levels of GluR2 were lower while the levels of GluR1, Beclin-1 and LC3 were higher significantly in HIBD group (P<0.05). The protein levels of LC3, Beclin-1, GluR1 and GluR2 in hippocampus tissues of HIBD group were significantly different among different time points after the establishment of HIBD model (F=10.65~701.14, P<0.01). The protein level of GluR2 was decreased from 1 h to 24 h after HIBD and reached the lowest level at 24 h. The levels of GluR1, Beclin-1 and LC3 were increased at 6 h, plateaued at 24 h and remained there until 48 h. The levels of these proteins returned back to the initial level at 72 h. Conclusions Ca-A/K channel-related molecules GluR2 and GluR1 play important roles in the autophagic cell death of hippocampus tissues in neonatal rats with hypoxic-ischemic brain damage.