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作 者:王进[1] 乔礼芬[2] 李永胜[1] 杨光田[1]
机构地区:[1]华中科技大学同济医学院附属同济医院急诊科,武汉430030 [2]华中科技大学同济医学院附属同济医院呼吸科,武汉430030
出 处:《中国药学杂志》2009年第13期993-996,共4页Chinese Pharmaceutical Journal
基 金:湖北省科技攻关计划项目(2003AA301C51)
摘 要:目的探讨参附注射液(SF)对大鼠肠缺血-再灌注(II/R)引起的远隔器官肺脏损伤的保护作用。方法通过夹闭肠系膜上动脉60min,再灌注120min,建立II/R损伤模型。实验大鼠随机分为4组:假手术组;II/R组;低剂量SF预处理组(SF-5组,5mL·kg-1);高剂量SF预处理组(SF-10组,10mL·kg-1)。观察各组大鼠肺组织丙二醛(MDA)、髓过氧化物酶(MPO)、肿瘤坏死因子-α(TNF-α)水平,肺脏组织H-E染色,ICAM-1和NF-κB表达。结果II/R组肺组织中MDA、MPO、TNF-α水平明显高于假手术组(P<0.05),ICAM-1与NF-κB表达明显高于假手术组(P<0.05),镜检发现肺组织有明显组织形态学损伤。与II/R组比较,SF能够降低肺组织中MDA、MPO、TNF-α水平(P<0.05);减少肺组织NF-κB和ICAM-1的表达(P<0.05);减轻肺脏组织形态学损伤。结论SF通过抑制NF-κB的激活,减少肺组织ICAM-1的表达和中性粒细胞的聚集,从而减轻II/R引起的肺脏损伤。OBJECTIVE To investigate the protective effects of Shcn-fu injection (SF) on lung injury induced by intestinal ischcmia rcpcrfusion (I/R) in rats. METHODS The intestinal ischcmia rcpcrfusion (I/R) model was established by superior mcscntcric artery (SMA) occlusion. Wistar rats wcrc randomly divided into four groups as follows: (i) control, sham operated group; (ii) I/R group (II/R group); (iii) group prctrcatcd with 5 mL·kg^-1 Shen-fu injection (SF-5 group); and (iv) group prctrcatcd with 10 mL·kg^-1 Shen-fu injection (SF-10 group). Lung histology was observed. Myclopcroxidasc (MPO) activity, Tumor necrosis factor α (TNF-α) and malondialdchydc (MDA) level in lung tissues and the immunohistochemical expression of lung ICAM-1 wcrc assayed. In addition, the Western blot of lung NF-κB was performed. RESULTS Compared with the sham-operated control group, lung injury was induced by intestinal I/R, characterized as histological damage including ocdcma, hacmorrhage and infiltration by inflammatory cells. Compared with the control group, MPO activity, TNF-α and MDA content in the lung tissues were increased significantly in the II/R group. Strong positive expression of lung ICAM-1 was observed. Compared with IFR group, administration of 5 and 10 mL·kg^-1 Fu rnarkcdly ameliorated lung injury. Compared with the II/R group, MPO activity, TNF-α and MDA contents in lung tissues wcre decreased significantly following Shcn-Fu prc-treatment, and the expression of lung NF-κB and ICAM-1 was markedly amelinratcd. CONCLUSION The present study reveals that Shen-Fu relieves lung injury induced by intestinal I/R. One possible mechanism responsible for this effect is the inhibition of ICAM-1 expression and neutrophil infiltration by inhibition of NF-κB activity.
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