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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 effect of LBP inhibitor P12 on the activity of nuclear factor kappa B (NF-κB) in lipopolysaccharide (LPS) -induced lung injury induced by lipopolysaccharide (LPS) in mice and to explore the mechanism by which P12 block endotoxin signal transduction pathway. Forty mice were randomly divided into five groups: control group, endotoxemia group, low dose P12 group, middle dose P12 group and high dose P12 group, with 8 mice in each group. The model of LPS-induced endotoxemia was established by intraperitoneal injection of LPS, P12 was injected into the caudal vein, the activity of NF-κB in lung tissue was determined by immunocytochemical staining and Western blot. The nitrate reductase Serum NO content. Results: After LPS stimulation, NF-κB P65 entered the nucleus and the nuclear translocation of P12 group was significantly decreased. The gray density (OD) of P65 nucleus in low, medium and high dose P12 groups were 1.45 ± 0.53, 1.24 ± 0.34 and 0.84 ± 0.75 respectively, significantly lower than those in endotoxemia group (3.08 ± 0.16). The levels of NO in low, middle and high dose P12 group were (106.17 ± 24.93) μmol / L, (80.84 ± 19.23) μmol / L and (67.28 ± 16.67) μmol / L respectively), which were significantly lower than those in endotoxemia group 20.13) μmol / L. P12 could significantly inhibit LPS-induced activation of NF-κB in lungs of mice with endotoxemia and reduce its release of NO. P12 endotoxemia may show that there may be a potential preventive and early treatment.