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机构地区:[1]复旦大学附属中山医院青浦分院急诊科,上海青浦201700
出 处:《湖北科技学院学报(医学版)》2015年第3期185-187,F0002,共4页Journal of Hubei University of Science and Technology(Medical Sciences)
基 金:上海市青浦区科委基金项目(2011-29)
摘 要:目的以内毒素(lipopolysaccharide,LPS)诱导法建立全身炎症反应综合征(SIRS)大鼠心肌损伤模型,探讨不同浓度硫辛酸(lipoic acid,LA)对大鼠心肌损伤的保护作用。方法选择健康SD大鼠75只,其中60只腹腔注射内毒素25mg/kg,构建SIRS大鼠心肌损伤模型,再分为阴性对照组、LA大剂量组、LA中剂量组、LA小剂量组,每组15只;其余15只大鼠为正常组。分别于24、48、72h后采用real-time PCR检测各组每只大鼠心肌组织中核因子κB(nuclear factor kappa B,NF-κB)、白细胞介素1(interleukin 1,IL-1)水平,ELISA法检测肿瘤坏死因子(tumor necrosis factorα,TNF-α)的水平。同时观察心肌组织变化。结果 LPS诱导后,LA阴性对照组大鼠心肌中NF-κB、IL-1、TNF-α在72 h时最高。与阴性对照组比较,处理24、48、72h后,LA大剂量组、中剂量组中NF-κB、IL-1、TNF-α表达水平下降(P<0.05);随硫辛酸剂量加大,心肌组织炎症反应相应减轻。结论硫辛酸对SIRS大鼠心肌损伤有一定保护作用,其机制可能与抑制NF-κB激活以及下调心肌组织中IL-1、TNF-α的表达有关。ABSTRACT:Objective To explore the protective effects of different dose of lipoic acid onmyocardial inju-ry rats with systemic inflammatory response syndrome ( SIRS) induced by lipopolysaccharide .Methods A total of 75 healthy SD rats were enrolled .Among them,60 rats were intraperitoneally injected with 25mg/kg LPS to establish SIRS model of myocardial injury ,thenthose rats were divided into negative control group ,LA high-dose group ,LA middle-dose group and LA low-dose group ,15 rats in each group .the other 15 rats were intraperitone-ally injected with saline solution ( normal group ) .The levels of NF-κB and IL-1 in myocardium were detected with real-time PCR after 24h,48h and 72h,respectively,and the level of TNF-αwas measured with ELISA.HE staining was used to observe the microscopical change of myocradium tissue .Results After challenge with LPS , the levels of NF-κB,IL-1 and TNF-αin myocardium in negative control group were the highest at 72h.Com-pared with the negative control group ,the levels of NF-κB,IL-1 and TNF-αin LA high-dose group and LA mid-dle-dose group were decreased after treatment for 24h,48h and 72h(P〈0.05).With LA dose increase,myo-cardial tissue inflammation reduced accordingly .Conclusion Lipoic acid has a protective effect on myocardial injury of SIRS rats,and the underlyingmechnism may be correlated with inhibition of NF-κB activation and the down-regulation of IL-1 and TNF-αexpression .
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