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目的 探讨内毒素血症时血浆氧化型低密度脂蛋白 (Ox -LDL)的变化规律及Ox -LDL对库普弗细胞 (KC) -内毒素 (LPS)反应的影响。 方法 Wistar大鼠 3 6只 ,随机分为对照组( 6只 )和LPS组 (分为 1,5 ,10mg kg三组 ,每组 10只 ) ,复制大鼠内毒素血症模型 ,采用ELISA方法检测对照组及注射内毒素后 0 .5 ,1,3 ,5 ,8h时血浆Ox -LDL水平变化及其与LPS的量效关系。分离培养小鼠KC ,分别用Ox-LDL( 10～ 10 0 μg ml)、抗小鼠清道夫受体 (SR)单抗 ( 10 μg ml)及抗CD14单抗 ( 10 μg ml) +Ox -LDL( 10 0 μg ml)预处理KC 1h后 ,再分别与 1,10ng mlLPS孵育 3h ,观察以上预处理对LPS诱导KC释放肿瘤坏死因子 -α(TNF -α)的影响及其与KC表面CD14的关系。细胞上清TNF -α水平采用ELISA法检测。 结果 注射LPS后 ,3组大鼠血浆Ox -LDL水平均显著增高 ,以 10mg kg组升高最明显。Ox -LDL预处理KC ,能显著增强内毒素对KC的激活作用 ,表现为TNF -α含量明显升高 ,呈明显的量效关系。Ox -LDL的这种增强作用与抗SR抗体影响LPS刺激KC的作用相同 ,而抗CD14抗体可完全抑制Ox-LDL的这种增强作用。 结论 内毒素血症早期血浆Ox-LDL水平明显增高 ,与LPS呈明显的量效关系 ;Ox -LDL能明显增强LPS对KC的激活作用 ,其机制可能与促进LPS
Objective To investigate the changes of plasma oxidized low density lipoprotein (Ox-LDL) and the effect of Ox-LDL on KC-LPS in endotoxemia. Methods Thirty six Wistar rats were randomly divided into control group (n = 6) and LPS group (divided into three groups of 1, 5 and 10 mg, with 10 rats in each group). Rat models of endotoxemia were duplicated. The levels of plasma Ox-LDL at 0, 5, 1, 3, 5, 8h after injection of endotoxin and the control group were measured, Mouse KC was isolated and cultured. Oxidized LDL (10 ~ 100 μg ml), anti - scandral receptor (SR) monoclonal antibody (10 μg ml) and anti - CD14 monoclonal antibody LDL (100 μg ml) for 1 h, then incubated with 1 and 10 ng ml LPS for 3 h respectively. The effect of the above preconditioning on the TNF-α release from LPS-induced KC and the relationship between CD14 Relationship. The level of TNF-α in cell supernatant was detected by ELISA. Results After injection of LPS, the levels of plasma Ox-LDL in the three groups were significantly increased, the most obvious increase in 10mg kg group. Ox-LDL pretreatment KC, can significantly enhance the activation of endotoxin KC, the performance of TNF-α was significantly increased, showing a significant dose-effect relationship. This enhancement of Ox-LDL is the same as the effect of anti-SR antibody on LPS-stimulated KC whereas anti-CD14 antibody completely inhibits this potentiation of Ox-LDL. Conclusions The level of Ox-LDL in early stage of endotoxemia is significantly increased, which shows a dose-effect relationship with LPS. Ox-LDL can significantly enhance the activation of KC by LPS, which may be related to the promotion of LPS