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作 者:张红梅[1] 李义召[2] 王凤山[3] 程艳娜[3] 夏作理[2]
机构地区:[1]山东省济南市第四人民医院神经内科,山东济南250031 [2]泰山医学院微循环研究所 [3]山东大学药学院
出 处:《中国医师杂志》2006年第11期1456-1458,1461,共4页Journal of Chinese Physician
基 金:国家自然科学基金资助项目(30270492)
摘 要:目的观察低分子肝素-超氧化物歧化酶(LMWH-SOD)对沙土鼠脑缺血再灌注脑组织肿瘤坏死因子α(TNF-α)表达的影响,探讨LMWH-SOD脑保护作用机制。方法健康沙土鼠48只,随机分为假手术组、生理盐水组、低分子肝素(LMWH)组、超氧化物歧化酶(SOD)组、LMWH与SOD联合(LMWH+SOD)治疗组和LMWH-SOD组。建立沙土鼠全脑缺血再灌注损伤模型,采用免疫组织化学染色法检测脑缺血10 m in再灌注6 h沙土鼠脑组织内TNF-α表达的变化。结果脑缺血再灌注后脑组织内TNF-α的表达明显升高;与生理盐水组比,各用药组TNF-α阳性细胞数明显减少(P<0.01),细胞染色明显变浅;而LMWH-SOD对TNF-α表达的抑制最为显著,阳性细胞数减少最为明显,与其它用药组比较差异有统计学意义(P<0.01),细胞着色也较浅。结论LM-WH-SOD对脑缺血再灌注损伤有保护作用,其脑保护机制可能与抑制炎性细胞因子TNF-α的过度表达有关。Objective To study the effect of LMWH-SOD on tumor necrosis factor-α(TNF-α) protein expression and its mechanism of brain protective action after cerebral ischemia-reperfusion in gerbils. Methods Eighteen gerbils were divided randomly into sham operation group, normal saline(NS) group and LMWH groups,SOD group, LMWH + SOD group and LMWH-SOD group. The experimental animal model of the global cerebral ischemia-reperfusion was established. The expression of TNF-α was observed by immunohistochemistry staining. Results In brain tissues, TNF-ct was significantly elevated after cerebral ischemia-reperfusion. The number of TNF-α positive cells were decreased in treated groups when compared with NS group ( P 〈0. 01 ). In LMWH-SOD group, TNF-α expression level was the lowest, the number of TNF-α positive cells was significantly reduced compared with other treated groups ( P 〈0. 01 ) , and the staining showed low intensity. Conclusion LMWH-SOD has protective effect against cerebral ischemia-reperfusion injury in gerbils possibly by inhibiting TNF-α expression.
关 键 词:肝素 低分子量 超氧化物歧化酶 脑缺血 再灌注 肿瘤坏死因子Α
分 类 号:R743[医药卫生—神经病学与精神病学] R96[医药卫生—临床医学]
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