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三七总皂苷对失血性休克模型大鼠在复苏期的保护作用及机制研究 被引量:2

Protective effect of Panax notoginseng saponins on rat model of hemorrhagic shock and resuscitation phase
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摘要 目的研究三七总皂苷对大鼠失血性休克复苏期的保护作用及机制。方法参与实验鼠失血75 min再灌注林格氏液达血容量90%造成失血休克复苏模型。取雄性Wistar大鼠100只,均分为对照组,模型组(失血性休克/复苏)以及三七总皂苷低、中、高剂量组(50,100,200 mg/kg),各组在失血性休克后70 min静脉注射给予相应剂量药物。除对照组外其他各组大鼠制备失血性休克模型,观察记录失血期以及复苏期动脉血氧分压、平均动脉血压和心率的变化,并在复苏期30 min以及2 h检测炎症因子TNFα、IL-1β以及内毒素、丙二醛(MDA)、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)的变化。结果三七总皂苷各个剂量组均可以升高复苏期大鼠的平均动脉压和氧动脉分压,降低TNFα、IL-1β的表达,减少血清MDA、内毒素和MPO水平,增强SOD的活性。结论三七总皂苷通过抗氧化应激以及抗炎的途径对失血性休克模型大鼠产生保护作用。 AIM To study the effect of Panax notoginseng saponins on an inflammatory response induced by hemorrhagic shock and resuscitation.METHODS The involved experimental rats model of hemorrhagic shock for 75 min and reperfusion of ringer’s solution up to 90% blood volume were created.One hundred male Wistar rats were randomly divided into five groups,control group,model group(hemorrhagic shock/resuscitation,HS/R) and Panax notoginseng saponins low,middle and high dose treatment groups(50,100,200 mg/kg).The does of Panax notoginseng saponins was injected at 70 min after hemorrhagic shock.Arterial oxygen pressure,mean arterial pressure and heart rate were recorded at hemorrhagic resuscitation phase.Then TNFα,IL-1β,endotoxin,malondialdehyde(MDA),superoxide dismutase(SOD) and myeloperoxidase(MPO) were tested in 30 min and 2 h after resuscitation.RESULTS Mean arterial pressure and arterial oxygen pressure in Panax notoginseng saponins treatment groups increased significantly(P<0.05).The inflammatory indexes in Panax notoginseng saponins treatment groups were lower than those in the model group in 30 min and 2 h.CONCLUSION Pretreatment of Panax notoginseng saponins before fluid resuscitation shows a beneficial effect on the hemodynamic stabilization through anti-inflammation and anti-oxidase in HS/R rat model.
作者 周志勇
出处 《中成药》 CAS CSCD 北大核心 2013年第3期436-440,共5页 Chinese Traditional Patent Medicine
关键词 三七总皂苷 失血性休克 复苏期 炎症因子 氧化应激 Panax notoginseng saponins hemorrhagic shock resuscitation phase cytokine oxidative stress
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