NR2A antisense oligonucleotide against cerebral ischemia - reperfusion and its mRNA expression in hippocampus of NR2A.doc

 PAGE \* MERGEFORMAT 20 NR2A antisense oligonucleotide against cerebral ischemia / reperfusion and its mRNA expression in hippocampus of NR2A Of: Zhang Xu, Liu Zhian, Teng big before, Gao Wei, Xu Tiejun [Abstract] Objective To study the NMDA receptor subunit 2A (NR2A) antisense oligonucleotide on ischemic / reperfusion rat hippocampal CA1 area and the mRNA expression of NR2A to explore the cerebral ischemia / Perfusion of hippocampal neurons induced by the possible mechanism of injury. Methods Male SD rats were randomly divided into normal control group, sham operation group and ischemia / reperfusion group. by saline, missense oligonucleotides and pretreated with antisense oligonucleotides to establish four-vessel occlusion transient forebrain ischemia (15 min) and reperfusion (24 h, 48 h and 72 h) animal model. in determining the time point perfusion fixed, drawing, embedded in paraffin and tissue sections (slice thickness 8 m), then underwent in situ hybridization and immunohistochemistry. The results of transient cerebral ischemia / reperfusion, the rat hippocampal CA1 area NR2A mRNA expression was significantly increased , compared with the control group significantly (P lt;0.05); NR2A antisense oligonucleotide significantly inhibited this increased expression (P lt;0.05). transient cerebral ischemia / reperfusion, a large hippocampal CA1 area NR2A protein expression was significantly reduced compared with the control group significantly (P lt;0.05); by NR2A antisense oligonucleotide pretreatment, to further enhance the reduction of NR2A expression, and control group difference was statistically significant (P lt;0.05). Conclusions transient cerebral ischemia / reperfusion in rat hippocampal CA1 area there is transcriptional enhancement of translation inhibition. NR2A antisense oligonucleotide can specifically inhibited the increase in NR2A mRNA expression, and can enhance the expression of NR2A decreased. NR2A antisense oligonucleotides of this effe