烫伤大鼠肝脏脂多糖结合蛋白和脂多糖受体CD14mRNA表达的意义

The significance of the expressions of lipopolysaccharide binding protein mRNA and lipopolysaccharide receptor CD14 mRNA in the liver of burned rat.

目的 观察烫伤后肠源性内毒素移位与肝组织内毒素增敏系统———脂多糖结合蛋白/脂多糖受体CD14(LBP/CD14)的相互关系及其意义。 方法 采用大鼠 35 %TBSAⅢ度烫伤模型 ,动物随机分为正常对照组、烫伤和重组杀菌 /通透性增加蛋白治疗组。烫伤组和rBPI2 1 治疗组动物于伤后 12h活杀。留取肝组织和血标本分别检测组织LBP、CD14、肿瘤坏死因子α(TNFα)mR NA表达及肝脏功能指标。 结果 烫伤后肝组织内毒素含量显著降增高 (P <0 .0 1) ,且肝组织LBP/CD14、TNFαmRNA表达亦明显增多。给予rBPI2 1 治疗可显著降低肝组织内毒素水平 ,并不同程度抑制组织LBP/CD14、TNFα基因表达。同时 ,rBPI2 1 治疗组动物血清谷丙转氨酶水平显著降低 (P <0 .0 1)。 结论 烫伤后移位内毒素聚积于肝脏 ,可明显刺激机体局部组织LBP/CD14mRNA的表达 。

Objective To explore the significance and the correlation between enteric endotoxin translocation and hepatic endotoxin-sensitivity-enhancing system─lipopolysaccharide-binding protein(LBP)/lipopolysaccharide receptor CD14(LBP/CD14) after burn. Methods Wistar rats subjected to 35% Ⅲ degree burn were employed as the model. The rats were randomly divided into three groups: i.e. normal control( C, n=8) group, thermal injury (T, n=10) group and recombinant bactericidal/permeability-increasing protein(rBPI 21 ) treatment (R, n=6) group. The rats in T and R groups were sacrificed at 12 postburn hour (PBH) and the liver tissue was collected for the detection of the mRNA expressions of LBP, CD14 and tumor necrosis factor(TNFα) and blood samples collected for hepatic functional indices. Results The hepatic endotoxin content increased significantly postburn (P < 0.01),and the expressions of LBP/CD14 and TNFα mRNA in liver tissue increased obviously. However the use of rBPI 21 could evidently lower hepatic endotoxin content and inhibit the expression of tissue LBP/CD14 and TNFα. In addition, rBPI 21 could also significantly decrease serum level of glutamic-pyruvic transaminase (ALT) (P < 0.01). Conclusion Aggregation of endotoxin in liver due to postburn translocation might obviously stimulate the expression of LBP/CD14 mRNA locally. The up-regulation of the expression of LBP/CD14 might be the principle molecular basis enhandced activity of translocated endotoxin on inflammatory cells.