摘要
目的:观察正常肠淋巴液对内毒素休克小鼠内毒素增敏系统的作用,探讨正常淋巴液干预内毒素休克小鼠器官损伤的作用机制。方法:36只SPF级BALC/c雄性小鼠18只采用常规方法引流正常肠淋巴液,另外18只分为假休克组(SS组)、内毒素休克模型组(ES组)和肠淋巴液干预组(NML+ES组),每组6只。后两组应用腹腔注射脂多糖(LPS,35mg/Kg)方法复制小鼠ES模型;60min后,NML+ES组小鼠经股动脉注射正常肠淋巴液(全血量的1/15);6h后摘取各组小鼠的肝、心肌和肺组织,制备组织匀浆,采用ELISA检测脂多糖结合蛋白(LBP)、脂多糖受体(CD14)、肿瘤坏死因子(TNF-α)和白介素6(IL-6)含量。结果:ES组肺、肝、心肌匀浆的LBP、CD14、TNF-α、IL-6含量均显著高于SS组(P<0.05);NML+ES组肺组织LBP和TNF-α、肝组织TNF-α和IL-6以及心肌组织LBP、CD14、TNF-α、IL-6含量均较ES组明显降低(P<0.05),但肝组织CD14及TNF-α、心肌组织CD14仍高于SS组。结论:正常肠淋巴液可降低内毒素休克小鼠肺、心肌组织内毒素增敏系统的LBP、CD14水平,从而降低炎症反应。
Objective:To observe the role of normal mesenteric lymph(NML)on the sensitization system of endotoxin in mice with endotoxic shock(ES),and investigate the mechanism of NML alleviating organ injury subjected to ES.Method:The NML was drained form 18health male BALC/c mice for the intervention of ES.The other 18mice were divided into the sham shock(SS),endotoxic shock(ES),and NML+ES groups,n=6.The ES model was established using the method of the intraperitoneal injection of lipopolysaccharide(LPS,35mg/Kg).After 60 min of LPS injection,the administration of NML(1/15of whole blood volume)was performed through femoral artery in the NML+ES group.At 6hafter intraperitoneal injection of LPS or corresponding time point,the lung,heart,and liver tissue specimens from a fixed location were harvested from each mouse for the measurement of lipopolysaccharide-binding protein(LBP),lipopolysaccharide receptor(CD14),tumor necrosis factor-α(TNF-α),and interleukin 6(IL-6)with enzyme-linked immunosorbent assay method.Results:The contents of LBP,CD14,TNF-α,and IL-6in lung,liver and myocardium in the ES group were increased significantly than those in the sham shock group.NML administration reduced the LBP and TNF-αcontents in lung,TNF-αand IL-6in liver,LBP,CD14,TNF-α,and IL-6in myocardium;meanwhile,the contents of CD14and TNF-αin liver,CD14in myocardium in the NML+ES group were also increased compared to the sham shock group.Conclusion:NML decreased the levels of LBP and CD14,a sensitization system of endotoxin,in lung and myocardium in mice with ES;as a result,reduced the inflammatory response.
出处
《微循环学杂志》
2014年第1期9-11,14,I0001,共5页
Chinese Journal of Microcirculation
基金
河北省教育厅科学研究项目(2007407
2005311)