›› 2014, Vol. 32 ›› Issue (4): 368-371.

• Original Article • Previous Articles     Next Articles

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

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.