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作 者:高永红[1] 袁拯忠[2] 牛福玲[1] 朱陵群[1] 李澎涛[3] 王硕仁[1]
机构地区:[1]北京中医药大学东直门医院,北京100700 [2]温州医学院附属第一医院,温州325000 [3]北京中医药大学基础医学院,北京100029
出 处:《中华中医药杂志》2008年第3期197-200,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家重点基础研究发展规划项目课题(No.G1999055404)
摘 要:目的:观察培养的大鼠脑缺血再灌注损伤微血管内皮细胞体外黏附分子细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)表达的变化,探讨新清开灵注射液阻抑脑缺血炎症反应的作用途径。方法:采用分离脑微血管段并消化的方法体外培养大鼠脑微血管内皮细胞,氧糖剥夺法(Kreb液,95%N2+5%CO2)模拟缺血再灌注损伤,分别采用免疫细胞化学染色和RT-PCR方法半定量检测黏附分子ICAM-1、VCAM-1的蛋白mRNA表达和mRNA转录水平。结果:与正常组比较,模型组ICAM-1、VCAM-1的蛋白和mRNA表达均明显增高(P<0.05);与模型组比较,清开灵组显著降低其蛋白表达和VCAM-1 mRNA转录水平(P<0.05);新清开灵注射液对ICAM-1和VCAM-1的蛋白和mRNA表达都有明显的抑制作用(P<0.05)。结论:新清开灵注射液通过干预黏附分子表达而阻抑脑缺血损伤炎症反应。Objective: To observe the expression of cell adhesion molecules ICAM-1 and VCAM-1 of cultured rat brain microvascular endothelial cells(MVEC), expecting to explore the mechanisms of new QingKaiLing injection protecting brain from injury of inflammatory cascade in cerebral ischemia diseases. Methods: Rat cerebral M VEC were extracted by separating microvessel sections and collagenase enzymatic digesting, an in vitro ischemia reperfusion model was established (Kreb, 95% N2 + 5% CO2), the protein and m RNA expression of ICAM-1 and VCAM-1 were detected by using immunocytochemical stain and RT-PCR method. Results: The expression of adhesion molecules of model group were significantly higher than those of noral group(P 〈 0.05 );compared with the model group, QingKaiLing injection can reduce the protein expression and VCAM-1mRNA level obviously (P 〈 0.05 ); new QingKaiLing injection can depress the protein and mRNA expression of both ICAM-1 and VCAM- 1significantly( P 〈 0.05 ). Conclusion: The function of new QingKaiLing injection on inflammatory cascade in cerebral ischemial diseases is probably by intervention of the expression of adhesion molecules.
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