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目的 研究内毒素肝损伤时 ,枯否氏细胞 (Kupffercells,KC)逐步由免疫防御型转变为效应型致肝损伤的机理。方法 昆明种小鼠 72只 ,一次性尾静脉内注射不同剂量 (1mg/kg、 10mg/kg)大肠杆菌内毒素 (LPS) ,复制内毒素肝损伤模型。采用免疫组化方法观察小鼠肝脏清道夫受体 (scavengerreceptor,SR)、CD14表达变化 ;酶联免疫吸附法 (ELISA)测定肝组织肿瘤坏死因子 (TNF -α)、白介素 - 6(IL - 6 )的水平 ,光镜观察肝组织学变化。结果 内毒素肝损伤过程中 ,KC表面SR表达呈进行性下调 ,且与内毒素呈明显的量效关系 ;KC表面CD14表达呈进行性上调 ,但加大内毒素剂量并未使其进一步增加。SR表达的平均光密度值 (OD值 )与肝组织TNF -α、IL - 6及血浆丙氨酸氨基转移酶 (ALT)、总胆红素(TBIL)呈显著的负相关 ,CD14表达的平均OD值与肝组织TNF α、IL 6及血浆ALT、TBIL水平呈显著的正相关。结论 内毒素肝损伤过程中 ,枯否氏细胞SR表达下调 ,CD14表达上调可能是枯否氏细胞由免疫防御细胞转化为致炎效应细胞导致肝损伤的机制之一。
Objective To study the mechanism of Kupffer cells (KC) gradually changing from immunologic defense to efferent liver injury during endotoxin liver injury. Methods Totally 72 Kunming mice were injected with LPS (1mg / kg, 10mg / kg) into the tail vein of a single injection, and endotoxin-induced liver injury was induced. The expression of scavenger receptor (SR) and CD14 in liver of mice was observed by immunohistochemical method. The levels of tumor necrosis factor (TNF - α), interleukin - 6 (IL - 6) in liver tissues were detected by enzyme linked immunosorbent assay (ELISA) ) Levels, light microscopy liver histological changes. Results During endotoxic injury of liver, the expression of SR on KC surface was down-regulated and showed a dose-response relationship with endotoxin. The expression of CD14 on KC surface was up-regulated, but the increase of endotoxin dose did not increase the expression of SR. The average optical density (OD) value of SR expression was negatively correlated with TNF - α, IL - 6 and ALT and TBIL in liver tissue, while the average of CD14 expression There was a significant positive correlation between OD value and TNFα, IL 6, ALT and TBIL levels in liver tissue. Conclusions During endotoxin induced liver injury, the expression of SR is down-regulated in Kupffer cells, and the up-regulation of CD14 may be one of the mechanisms of Kupffer cells’ transformation from immune defensive cells to proinflammatory cells.