Wittner M, Sivenius J, Koistinaho J
Department of Neurology, University of Kuopio, Finland.
Neurosci Lett. 1997 Aug 29;232(2):75-8. doi: 10.1016/s0304-3940(97)00585-5.
The effect of dexmedetomidine, a selective alpha2-adrenoreceptor agonist and neuroprotective agent on the expression of immediate early genes and heat shock protein hsp70, was studied using quantitative in situ hybridization in a global ischemia model. At the dose previously shown to be neuroprotective dexmedetomidine inhibited the expression of c-fos and hsp70 mRNA, did not affect jun-B mRNA, and enhanced the induction of NGFI-A mRNA in the postischemic gerbil hippocampus. The reduced gene expression of c-fos and hsp70 was detected in the CA1 pyramidal cells which are prone to ischemic degeneration, whereas the increased gene expression of NGFI-A was measured from the CA3 and dentate gyrus, areas relatively resistant to ischemia. These alterations in early gene expression possibly reflect the mechanisms mediating the neuroprotective effects of alpha2-adrenoreceptor agonists.
在全脑缺血模型中，使用定量原位杂交技术研究了选择性α2-肾上腺素能受体激动剂和神经保护剂右美托咪定对即刻早期基因和热休克蛋白hsp70表达的影响。在先前显示具有神经保护作用的剂量下，右美托咪定抑制了沙土鼠缺血后海马体中c-fos和hsp70 mRNA的表达，不影响jun-B mRNA的表达，并增强了NGFI-A mRNA的诱导。在易发生缺血性变性的CA1锥体细胞中检测到c-fos和hsp70的基因表达降低，而从对缺血相对耐受的CA3和齿状回区域测量到NGFI-A的基因表达增加。早期基因表达的这些改变可能反映了介导α2-肾上腺素能受体激动剂神经保护作用的机制。
