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作 者:符荣[1] 赵甲山[1] 赵洪洋[1] 朱贤立[1] 陈衔城[2]
机构地区:[1]华中科技大学同济医学院附属协和医院神经外科,武汉430022 [2]复旦大学附属华山医院神经外科
出 处:《临床神经病学杂志》2004年第6期441-443,i001,共4页Journal of Clinical Neurology
摘 要:目的 研究血红素氧合酶 1(HO 1)及血红素氧合酶 2 (HO 2 )在局灶性脑缺血中的作用。方法 采用大鼠大脑中动脉栓塞脑缺血模型 ,对 6 6只大鼠脑缺血后不同时间点进行HO 1、HO 2免疫组化染色及病理学研究 ,并用计算机图像分析技术计算两者表达水平。结果 栓塞后 30min大鼠皮质及海马即有HO 1阳性神经元及胶质细胞的表达 ,且随着时间推移HO 1的表达逐渐增强 ,到栓塞后 12h达峰值 (P <0 0 1) ,以后逐渐下降 ,栓塞后 1周仍有HO 1表达。HO 2在正常大鼠及梗死大鼠脑组织内均有表达。栓塞后不同时间段 ,HO 2阳性神经元的数量无明显变化 (P >0 0 5 ) ,但HO 2表达呈动态变化 ,2 4h时最高 (P <0 0 1) ,以后逐渐下降。结论 脑缺血时脑内HO 1、HO 2表达的不同变化 ,是脑组织对损伤恢复重要的机制之一。HO 1修复受损的神经元和胶质细胞 ,而HOObjective To study the different role of heme oxygenase-1 (HO-1) and heme oxygenase-2 (HO-2) protein during permanent focal cerebral ischemia in rats.Methods Focal cerebral ischemic models of rat were made by middle cerebral artery occlusion (MCAO). The expression of heme oxygenase-1 and heme oxygenase-2 protein in the brains in 66 rats during different time was investigated by using immunohistochemistry, pathological study and computer image. Results HO-1 positive expression both in neurons and gliocytes was observed in the collateral cerebral cortex infarction area and hippocampus 30 min after MCAO. With time going on, the expression of HO-1 protein increased, peaked at 12h ( P<0.01) and then drop off, lasted till 7d after MCAO. HO-2 expression was observed both in normal rats and rats with infarction. There was no change of the number of HO-2 positive neurons in different time ( P>0.05). But HO-2 protein expression fluctuated, and peaked at 24h ( P<0.01), then descended.Conclusions The different expression of HO-1 and HO-2 is one of the important mechanism of cerebral tissue recovery from ischemic injury in permanent focal cerebral ischemia in rats. HO-1 and HO-2 protein plays different role in cerebral protection. HO-1 helps to repair damaged neural cells and HO-2 assists to maintain normal neural cell's structure and function stableness.
关 键 词:局灶性脑缺血 血红素氧合酶-1 血红素氧合酶-2
分 类 号:R743[医药卫生—神经病学与精神病学]
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