LBP抑制肽对LPS诱导的小鼠内毒素血症肺组织NF-κB活性的影响  

Effects of the inhibitory peptide of polysaccharide binding protein on the NF-κB activity of mouse lung tissues induced by LPS in a mouse model with endotoxemia

作　　者：吴学玲[1] 赵云峰[2] 徐德斌[1] 钱桂生[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸病研究所,重庆400037 [2]东南大学中大医院呼吸科,南京210009

出　　处：《现代免疫学》2009年第1期45-49,共5页Current Immunology

基　　金：国家自然科学基金资助项目(30170366)

摘　　要：研究LBP抑制肽P12对脂多糖(LPS)诱导的小鼠内毒素血症肺组织核转录因子κB(NF-κB)活性的影响,探讨P12体内阻断内毒素信号转导通路的部分机制。40只小鼠随机分为5组:对照组、内毒素血症组、低剂量P12组、中剂量P12组和高剂量P12组,每组8只。腹腔内注射LPS复制内毒素血症模型,尾静脉注射P12,用免疫细胞化学染色图象分析法和蛋白质定量分析法(Western blot)测定小鼠肺组织NF-κB的活性;硝酸还原酶法测定血清中NO的含量。结果:LPS刺激后NF-κB P65进入核内,P12组核易位明显减少。低、中、高剂量P12组P65核浆灰度(OD)比分别为1.45±0.53、1.24±0.34、0.84±0.75,明显低于内毒素血症组(3.08±0.16)。低、中、高剂量P12组NO水平分别为(106.17±24.93)μmol/L、(80.84±19.23)μmol/L和(67.28±16.67)μmol/L,明显低于内毒素血症组(185.49±20.13)μmol/L。P12能显著抑制LPS诱导的小鼠内毒素血症肺组织NF-κB的活化,并降低其NO的释放。表明P12对内毒素血症可能具有潜在的预防和早期治疗作用。To investigate the in vivo effects of a inhibitory peptide P12 of polysaccharide binding protein(LBP) on the activity of nuclear factor κB(NF-κB) in a mouse model with endotoxemia,40 mice of Kunming strain were randomly divided into 5 groups,i.e.control group,endotoxemia group,treated group with low-dose of P12,treated group with middle dose of P12 and treated group with high dose of P12,in which the endotoxemia group of mice was established by intraperitoneal injections of LPS and in the treated groups of ...

关 键 词：脂多糖结合蛋白抑制肽 脂多糖 核转录因子ΚB 一氧化氮 

分 类 号：R563[医药卫生—呼吸系统]