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机构地区:[1]大连大学附属中山医院急诊科,辽宁省大连116011 [2]大连医科大学附属第二医院神经内科
出 处:《中国基层医药》2007年第12期1976-1978,共3页Chinese Journal of Primary Medicine and Pharmacy
摘 要:目的研究缺血预处理后对再次脑缺血的神经功能、脑梗死体积以及脑组织中caspase-3表达的影响,探讨脑缺血预处理引起的脑保护机制。方法48只健康雄性Sprague-Dawley(SD)大鼠(体质量200~250 g)随机分两组:脑缺血组(n=24)和脑缺血预处理组(简称预处理组,n=24)。各组按再缺血时间6 h、1 d、2 d、4 d分为4个亚组。结果在缺血后相同时间点,预处理组比缺血组神经功能缺损评分明显减轻(P<0.05),梗死体积明显减小(P<0.05).caspase-3阳性细胞表达明显降低(P<0.05)。结论缺血预处理组对再次缺血可产生保护作用,减轻神经功能缺损症状,缩小梗死体积,减少caspase-3的表达.增强脑组织对脑缺血的耐受能力.提示抑制凋亡的发生可能是缺血预处理诱导脑缺血耐受的机制之一。Objective To investigate effects of cerebral ischemic preconditioning on neurological function,infarct volume,and the expression of caspase-3 in brain issue after brain ischemia again, and to investigate the brain protection mechanism produced by cerebral ischemia preconditioning. Methods 48 healthy male Sprague-Dawley (SD) rats( weighted 200-250g) were randomly divided into 2 groups: ischemia group( n = 24 ), ischemia precondi- tioning group ( namely preconditioning group,n= 24). Each group was divided into 4 subgroups according to 6h, 1d, 2d,4d after ischemia again. Results At the same point of time after ischemia,neurological deficit in preconditioning group was much less than that in ischemia group, the difference was significant(P 〈 0.05);brain infarct volume of the rats in preconditioning group was smaller than that of ischemia group, the difference was significant( P 〈 0.05) ; the expression of caspase-3 positive-cells was lower in preconditioning group than that in ischemia group( P 〈 0.05). Conclusion Cerebral ischemia preconditioning could protect the brain against ischemia again,decrease neurological deficits and infarct volume,inhibit the expression of caspase-3,and increase the tolerance of brain tissue to ischemia, the inhibition of apoptosis maybe one of the mechanisms that ischemia preconditioning induce ischemic tolerance.
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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