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Experimental study on the induction of acute hepatic injury by endotoxin
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- Author:
- No author available
- Journal Title:
- JOURNAL OF EMERGENCY MEDICINE
- Issue:
- 1
- DOI:
- 10.3760/j.issn:1671-0282.2002.01.002
- Key Word:
- 肝损伤;内毒素血症;清道夫受体;CD14;肿瘤坏死因子-α
Abstract： 目的研究内毒素肝损伤时,枯否氏细胞(Kupffer cells,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(scavenger receptor,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.
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