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作 者:贺斌峰[1] 海乐[2] 魏征华[1] 李瑾[1] 钱桂生[1] 王关嵩[1]
机构地区:[1]解放军第三军医大学新桥医院全军呼吸内科研究所军队及重庆市呼吸疾病重点实验室,重庆400037 [2]西南大学药学院,重庆400716
出 处:《中国急救医学》2012年第1期47-50,共4页Chinese Journal of Critical Care Medicine
基 金:军队“十一五”科技攻关课题(No.08G093)
摘 要:目的探讨七叶皂苷钠对模拟高原低氧大鼠脑损伤的干预作用及对水通道蛋白4(AQPg)表达的影响。方法40只SD大鼠随机均分为正常对照组、高原低氧致脑损伤组、七叶皂苷钠干预组。将大鼠放置在模拟海拔6000m高原环境中,每6h舱外以20m/min运动2h,重复三次致大鼠脑损伤。脑损伤后干预组给予尾静脉推注5mg/kg七叶皂苷钠,高原低氧致脑损伤组尾静脉推注5mg/kg生理盐水,分别观察各组脑组织病理切片、含水量、TNF—α含量和AQPd蛋白在脑组织中的定位及表达情况。结果病理切片显示,大鼠高原脑损伤后立即给予七叶皂苷钠干预,脑损伤程度显著减低。免疫组化示,AQP4蛋白主要在脑组织星形胶质细胞、小胶质细胞胞浆中呈阳性表达,且干预组较脑损伤组AQP4蛋白表达量显著降低;与正常组比较,脑损伤组12h脑含水量、TNF-α含量和AQP4蛋白表达显著升高,干预组12h脑含水量、12hTNF-α含量和6、12hAQP4蛋白表达较脑损伤组显著降低。结论七叶皂苷钠通过抑制TNF-α及下调AQP4表达,从而有效改善高原脑损伤程度。Objective To investigate the effect of sodium aescinate on brain injury of simulated high altitude hypoxia rats and expression of AQP4. Methods 40 SD rats were randomly divided into three groups, which were normoxic, simulated high altitude hypoxia and sodium aescinate treatment group. Rats in two latter groups were exposed to simulated 6000 - meter altitude and were forced to walk on tred- mill at roughly 20 m/min for 2 h at intervals of 6 h, repeated three times to induce brain damage. After brain injury, rats in sodium aescinate treatment group were injected with 5 mg/kg sodium aescinate and rats in simulated high altitude hypoxia group were injected with 5 mg/kg NS in tail vein respectively. Histological measurements, water content, TNF - α concentration and location and expression of cerebral AQP4 were determined. Results The histology of brain showed that brain injury was significantly reduced by immediate sodium aescinate intervention. AQP4 protein positively expressed in cytoplasm of astroglia cells and microglia by immunohistochemistry, and was higher in simulated high altitude hypoxia group than in sodium aescinate treatment group. Compared with the nonnaxic group, 12 h cerebral water contents, TNF - α concentration and AQP4 expression were significantly higher in simulated high altitude hypoxia group at 6 h and 12 h. Compared with simulated high altitude hypoxia group, 12 h cerebral water contents and 12 h the levels of TNF - α were decreased significantly in sodium aescinate treatment group, and 6 h, 12 h AQP4 protein were significantly different between two groups. Conclusion Sodium aescinate ameliorates high - altitude brain injury by inhibiting TNF - α and down- regulating AQPd expression in rats.
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