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作 者:耿晓娟 张琳娜 Geng Xiaojuan;Zhang Linna(Intensive Care Unit,the Affiliated Hospital of Xuzhou Medical University,Xuzhou 221000)
机构地区:[1]徐州医科大学附属医院重症医学科,江苏徐州221000
出 处:《中国现代医药杂志》2017年第7期29-32,共4页Modern Medicine Journal of China
摘 要:目的研究选择性磷酸二酯酶4(PDE4)抑制剂咯利普兰对百草枯(PQ)中毒致小鼠急性肺损伤(ALI)的保护作用,初步探讨其作用机制。方法将雄性BALB/c小鼠150只随机分为对照组(Con组),PQ染毒模型组(Mod组),PQ染毒+0.1mg/kg Rol组(0.1Rol组),PQ染毒+0.3mg/kg Rol组(0.3Rol组),PQ染毒+1.0mg/kg Rol组(1.0Rol组),各组按染毒时间点又分为3h、6h、9h、12h和24h 5个亚组,每组6只。采用腹腔注射20%PQ溶液(45mg/kg)的方法制备急性PQ中毒所致小鼠ALI模型,Con组腹腔注射等容积生理盐水。染毒0.5h后,咯利普兰组分别腹腔注射不同剂量咯利普兰,Mod组与Con组腹腔注射等容积生理盐水。在染毒后第6小时处死小鼠取肺组织,检测肺组织c AMP含量,HE染色观察肺组织病理学改变。结果与Con组比较,Mod组、咯利普兰三组c AMP含量下降(P<0.05),病理显示炎性细胞浸润,肺泡塌陷等肺组织损伤性改变。与Mod组比较,咯利普兰组肺组织cAMP含量下降幅度较Mod组低(P<0.05),肺组织病理改变明显减轻。结论咯利普兰能明显减轻PQ诱导的ALI,其发挥保护作用与升高肺组织cAMP含量,抑制过度炎症反应有关。Objective To establish the paraquat induced acute lung injury in mouse and investigate the probable mechanism of Rolipram in the process of acute lung injury induced by paraquat poisoning.Methods150mouse were randomly divided into control group,model group,a dose of0.1mg/kg Rolipram group,a dose of0.3mg/kg Rolipram group,a dose of1.0mg/kg Rolipram group.The mouse in each group then were divided into five subgroups of3h,6h,9h,12h and24h(n=6).The mouse in the paraquat group and the treatment group were all injected intraperitoneally with paraquat(45mg/kg)to induce lung injury,the control group were injected with the same volume of normal saline.After the administration6h,killed the mouse and measured the concentration of cAMP;observed the pathology of lung tissue by HE staining.Results Compared with control group,the concentration of cAMP in lung tissue in model group and every treatment group significantly reduced(P<0.05).The concentration of cAMP in lung tissue of three treatment group was significantly higher than model group(P<0.05),compared with model group,the injury of Rolipram group significantly reduced.Conclusion Rolipram can improve the acute lung injury effectively induced by paraquat poisioning in mouse,its improvement is associated with reducing cAMP activity,inhibiting nuclear transcription factor and affecting the expression of inflammatory factor.
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