首页> 中文期刊> 《中国急救医学》 >内皮细胞特异性分子与炎症因子在脂多糖导致的小鼠急性肺损伤中的表达研究

内皮细胞特异性分子与炎症因子在脂多糖导致的小鼠急性肺损伤中的表达研究

         

摘要

Objective To explore endocan and inflammatory factors expression during lipopolysaccharide ( LPS) induced acute lung injury ( ALI ) in mice, and to explore their roles during ALI in mice.Methods LPS-induced mice ALI models were assigned into control groups and LPS groups (0, 6, 12, and 24 h according to time points pre-scheduled).The ALI models were injected with 5 mg/kg LPS through tail vein, and the normal control groups were administrated with equal volume phosphate buffer solution (PBS). Mice were anesthetized, and blood samples were collected.Mice were then killed; lungs were obtained to perform next experiments.Lung samples were processed and hemotoxylin and eosin staining ( HE ) were done to examine the histopathological changes. Myeloperoxidase ( MPO) and wet to dry of lungs were measured.Levels in mice serum of tumor necrosis factorα( TNF-α) , interlukin -6 ( IL -6 ) , high mobility group box1 ( HMGB1 ) were analyzed. Expression of nuclear factor-κB ( NF-κB) and phosphorylated nuclear factor-κB were tested by immunoblotting assays.Results Compared with the control groups, LPS administration resulted in severe lung injury, increased lung wet/dry ratio.MPO levels, expression of TNF -α, IL -6, and HMGB1were elevated significantly after LPS treatment.Meantime, LPS also increased endocan and phosphorylated NF -κB expression in mice.Conclusion The expression changes of inflammatory factors and endocan may suggest the development process during LPS induced lung injury.The present study may offer beneficial reference for treating ALI, and decreasing multiple organs failure ( MOF) in earlier phase clinically.%目的:探讨内皮细胞特异性分子与炎症因子在脂多糖( LPS)导致的小鼠急性肺损伤( ALI)中的表达水平变化,及其与ALI的关系。方法复制LPS导致的小鼠ALI模型,将小鼠分为对照组与模型组(按时间点分别分为0、6、12和24 h)。模型组给予尾静脉注射内毒素(5 mg/kg),正常组在相同时间点给予尾静脉注射等量的磷酸缓冲盐溶液( PBS),在各个时间点麻醉取血后处死,取肺脏标本,观察肺脏病理形态学变化,测定肺脏的湿/干质量比与髓过氧化物酶( MPO),酶联免疫试剂盒测定炎症因子包括肿瘤坏死因子-α( TNF-α)、白细胞介素-6( IL-6)、高迁移率族蛋白1(HMGB1)与内皮特异性分子的表达,免疫印迹法观察核转录因子-κB ( NF-κB)与磷酸化NF-κB的变化。结果与对照组比较,模型组的肺组织损伤严重,肺湿/干质量比明显增加,MPO与炎症因子TNF-α、IL-6、HMGB1表达明显升高,同时内皮特异性分子与磷酸化NF-κB表达也明显升高。结论内皮特异性分子与炎症相关因子的表达变化可能提示LPS导致的小鼠ALI的进展,为早期干预ALI、降低多器官功能失调的发生率提供有益的参考。

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