摘要
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 observe the changes of SR and CD14 expression on kupffer cells and study their role on pathogenesis of liver injury in mice.Mehtods 1mg/kg or 10mg/kg of E Coli 026:B6 LPS were injected as bolus via i v.to reproduce an animal model of endotoxin induced liver injury.The changes of SR and CD14 expression on KC were determined with immunohistochemistry.TNF-α,IL-6 level in hepatic tissue were assayed using ELISA.Results The expression of SR on kupffer cells was progressively down-regulated by LPS in a dose dependent fashion,while the expression of CD14 was gradually up-regulated,which was not significantly different among small and large-dose groups.TNF-α?IL-6 level in hepatic tissue and ALT,TBIL in plasma were significantly negatively correlated with the expression of SR,and positively with the expression of CD14.Conclusion The up-regulation of CD14 expression and down-regulation of SR on KC might be one of the important mechanisms of the conversion of KC from immune defensive to inflammatory response cells in acute hepatic injury. [
出处
《中华急诊医学杂志》
CAS
CSCD
2002年第1期6-9,共4页
Chinese Journal of Emergency Medicine
基金
国家自然科学基金资助项目 ( 39770 313)
