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作 者:邢海波[1] 李刚[2] 徐亚平[3] 高福云[3] 刘国玲[3]
机构地区:[1]绍兴市人民医院ICU,浙江绍兴312000 [2]卫生部中日友好医院ICU,北京100029 [3]卫生部中日友好医院临床医学研究所,北京100029
出 处:《中国呼吸与危重监护杂志》2009年第2期176-180,共5页Chinese Journal of Respiratory and Critical Care Medicine
摘 要:目的探讨自由基清除剂依达拉奉(ED)对脓毒症致ALI的保护作用。方法24只雄性Wistar大鼠随机分成3组:对照组(NS组)、模型组(LPS组)及依达拉奉治疗组(ED组)。LPS组和ED组采用尾静脉注射LPS(10 mg/kg)建立ALI模型,ED组随后立即尾静脉注射依达拉奉(3 mg/kg)。LPS注射6 h后留取肺标本,分别测定肺组织湿/干重比值(W/D)和肺组织匀浆中髓过氧化物酶(MPO)、丙二醛(MDA)和超氧化物歧化酶(SOD)含量,观察肺组织病理改变及肺组织核因子κB(NF-κB)表达情况。结果LPS组肺组织MPO、MDA含量、W/D、肺损伤评分及肺组织NF-κB表达均高于NS组(P均<0.01),肺组织SOD含量低于NS组(P<0.01)。ED组肺组织MPO、MDA含量、W/D、肺损伤评分及肺组织NF-κB表达均低于LPS组(P均<0.01),仍高于NS组(P均<0.01);ED组肺组织SOD含量高于LPS组(P<0.01),仍低于NS组(P<0.01)。结论依达拉奉可以减轻LPS诱导的大鼠ALI,其机制可能与清除ROS,降低了NF-кB信号转导通路的活化,进而减轻炎症级联放大效应有关。Objective To explore the potential protective effect in vivo of Edaravone,a free radical scavenger on model of acute lung injury in rats with sepsis. Methods Twenty-four male Wistar rats were randomly divided into three groups, ie. a control group( NS group) , a model group( LPS group) , a Edaravone treatment group( ED group). ALl was induced by injecting LPS intravenously( 10 mg/kg) in the LPS group and the ED group. Meanwhile the ED group was intravenously injected with Edaravone (3 mg/kg). The NS group was injected with normal saline as control. The lung tissue samples were collected at 6 h after intravenous injection. The wet/dry ( W/D ) weight ratio of lung tissue was measured. The levels of myeloperoxidase ( MPO ), malondialdehyde ( MDA ) and superoxide dismutase ( SOD ) in lung tissue homogenate were assayed. The pathological changes and expression of nuclear factor-kappa B ( NF-kB ) in lung tissue were also studied. Results Compared with the NS group, The W/D, pathological scores, NF-kB expression, MPO and MDA levels in the LPS group were significantly higher( all P 〈 0. 01 ) , and the level of SOD was apparently lower ( P 〈 0. 01 ). The W/D, pathological scores, NF-kB expression, MPO and MDA levels in the El) group were significantly lower than those in the LPS group( all P 〈 0. 01 ) and higher than those in the NS group( all P 〈0. 01 ). And the level of SOD in lung tissue of the ED group was higher than that in the LPS group and lower than that in the NS group ( P 〈 0. 01 ). Conclusions Edaravone has protective effect on ALI rat model. The mechanism may be related to its ability of clearing the reactive oxygen species, inhibiting the activation of the signal pathway of NF-kB and inflammatory cascade.
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