To investigate the underlying mechanism of the protection on cerebral ischemia of α2-adrenergic agonist clonidine. The cerebral ischemia rat model was made by right middle cerebral artery occlusion for 2 h and reperf...To investigate the underlying mechanism of the protection on cerebral ischemia of α2-adrenergic agonist clonidine. The cerebral ischemia rat model was made by right middle cerebral artery occlusion for 2 h and reperfu- sion for 4 h. The Sprague Dawley rats were randomly divided into the sham-operative group, the cerebral ischemia model group, the clonidine group, the yohimbine ＋ clonidine group and the yohimbine group. The results shown that neurological deficit scores of rats pretreated with clonidine before the ischemia were better than the sham-opera- tive group. Clonidine group had significantly reduced brain infarct volumes. Clonidine decreased the expression of phospho-NMDAR2B and increased the expression of phospho-NMDAR1 and NMDAR2A. Therefore, clonidine sig- nificantly alleviated cerebral ischemia / reperfusion injury. The mechanism may be related to the regulation of phos- pho-NMDAR2B, phospho-NMDAR1 and NMDAR2A during cerebral ischemia/reperfusion.展开更多
文摘To investigate the underlying mechanism of the protection on cerebral ischemia of α2-adrenergic agonist clonidine. The cerebral ischemia rat model was made by right middle cerebral artery occlusion for 2 h and reperfu- sion for 4 h. The Sprague Dawley rats were randomly divided into the sham-operative group, the cerebral ischemia model group, the clonidine group, the yohimbine ＋ clonidine group and the yohimbine group. The results shown that neurological deficit scores of rats pretreated with clonidine before the ischemia were better than the sham-opera- tive group. Clonidine group had significantly reduced brain infarct volumes. Clonidine decreased the expression of phospho-NMDAR2B and increased the expression of phospho-NMDAR1 and NMDAR2A. Therefore, clonidine sig- nificantly alleviated cerebral ischemia / reperfusion injury. The mechanism may be related to the regulation of phos- pho-NMDAR2B, phospho-NMDAR1 and NMDAR2A during cerebral ischemia/reperfusion.
