目的:探讨早期“强制性使用”对局灶性脑梗死大鼠大脑皮层微管相关蛋白-2(M A P-2)表达的影响。方法:70只W istar大鼠随机分为假手术(D)组(10只)和手术组(60只),后者制作成右侧大脑中动脉阻塞(M CAO)模型,24h后再分为患侧前肢固定(A)组...目的:探讨早期“强制性使用”对局灶性脑梗死大鼠大脑皮层微管相关蛋白-2(M A P-2)表达的影响。方法:70只W istar大鼠随机分为假手术(D)组(10只)和手术组(60只),后者制作成右侧大脑中动脉阻塞(M CAO)模型,24h后再分为患侧前肢固定(A)组、未固定(B)组和健侧前肢固定(C)组,每组20只。21天后解除固定,于M CA O后21天和28天时,用免疫组化的方法检测梗死灶周围大脑皮质M AP-2的表达。结果:与D组相比,手术组大鼠梗死灶周围皮质M AP-2阳性神经元数量明显减少,但光密度值增高(P<0.05或P<0.01);手术组大鼠梗死灶周围皮质M AP-2阳性细胞数及光密度值,B组高于A组,A组高于C组(P<0.05)。结论:脑缺血损伤可刺激M AP-2的表达,肢体固定或过度使用对梗死灶周围皮质部分神经元代偿性高表达M A P-2有不利影响,其中患侧前肢过度使用的影响尤其明显。展开更多
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
文摘目的:探讨早期“强制性使用”对局灶性脑梗死大鼠大脑皮层微管相关蛋白-2(M A P-2)表达的影响。方法:70只W istar大鼠随机分为假手术(D)组(10只)和手术组(60只),后者制作成右侧大脑中动脉阻塞(M CAO)模型,24h后再分为患侧前肢固定(A)组、未固定(B)组和健侧前肢固定(C)组,每组20只。21天后解除固定,于M CA O后21天和28天时,用免疫组化的方法检测梗死灶周围大脑皮质M AP-2的表达。结果:与D组相比,手术组大鼠梗死灶周围皮质M AP-2阳性神经元数量明显减少,但光密度值增高(P<0.05或P<0.01);手术组大鼠梗死灶周围皮质M AP-2阳性细胞数及光密度值,B组高于A组,A组高于C组(P<0.05)。结论:脑缺血损伤可刺激M AP-2的表达,肢体固定或过度使用对梗死灶周围皮质部分神经元代偿性高表达M A P-2有不利影响,其中患侧前肢过度使用的影响尤其明显。
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.
