• 重慶醫(yī)科大學(xué)附屬第二醫(yī)院普通外科（重慶400010）;;
  • 通訊作者: 龔建平;

目的探討內(nèi)毒素血癥時(shí)大鼠肝組織中脂多糖結(jié)合蛋白mRNA的表達(dá)、血漿中脂多糖結(jié)合蛋白(LBP)含量的變化及其意義。方法經(jīng)大鼠尾靜脈注入內(nèi)毒素（5 mg/kg）建立內(nèi)毒素血癥動(dòng)物模型，檢測(cè)不同時(shí)點(diǎn)模型鼠肝組織中LBP mRNA的表達(dá)，同時(shí)檢測(cè)血漿中LBP、內(nèi)毒素、TNFα及IL6含量的變化，并與對(duì)照組相比較。另取肝組織在電鏡下觀察其病理學(xué)改變。結(jié)果隨著內(nèi)毒素血癥時(shí)間的延長(zhǎng)，內(nèi)毒素組大鼠肝組織LBP mRNA的表達(dá)明顯增強(qiáng)，血漿中LBP、TNFα和IL6含量也明顯增加，與對(duì)照組比較差異有高度顯著性（P＜0.01）。電鏡觀察見(jiàn)肝細(xì)胞脂肪變，線粒體空化，枯否氏細(xì)胞數(shù)量增多、體積增大、吞噬功能增強(qiáng)。結(jié)論內(nèi)毒素血癥時(shí)，大鼠肝組織中LBP mRNA表達(dá)明顯增強(qiáng)，血漿中LBP含量也明顯增加。由此提示，增高的LBP可能在脂多糖介導(dǎo)的枯否氏細(xì)胞激活及產(chǎn)生、釋放各種炎性介質(zhì)中可能起了重要作用。

引用本文： 涂兵,龔建平,石毓君,李旭宏,劉長(zhǎng)安,李生偉. 內(nèi)毒素血癥時(shí)大鼠脂多糖結(jié)合蛋白的變化及其意義. 中國(guó)普外基礎(chǔ)與臨床雜志, 2003, 10(4): 355-358. doi: 復(fù)制

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2. Heumann D, Adachi Y, Le Roy D, et al. Role of plasma, lipopolysaccharidebinding protein, and CD14 in response of mouse peritoneal exudate macrophages to endotoxin [Ｊ]. Infect Immun, 2001; 69(1)∶378.
3. Gong JP, Wu CX, Liu CA,et al. Intestinal damage mediated by Kupffer cells in rats with endotoxemia [Ｊ]. World J Gastroenterol， 2002; 8(5)∶923.
4. Vreugdenhil AC, Dentener MA, Snoek AM, et al. Lipopolysaccharide binding protein and serum amyloid A secretion by human intestinal cells during the acute phase response [Ｊ]. J Immunol,1999; 163(5)∶2792.
5. Erwin PJ, Lewis H, Dolan S, et al. Lipopolysaccharide binding protein in acute pancreatitis [Ｊ]. Crit Care Med, 2000; 28(1)∶104.
6. Clark JG, Madtes DK, Martin TR, et al. Idiopathic pneumonia after bone marrow transplantation: cytokine activation and lipopolysaccharide amplification in the bronchoalveolar compartment [Ｊ]. Crit Care Med,1999; 27(9)∶1800.
7. Le Roy D, Di Padova F, Tees R, et al. Monoclonal antibodies to murine lipopolysaccharide (LPS)binding protein (LBP) protect mice from lethal endotoxemia by blocking either the binding of LPS to LBP or the presentation of LPS/LBP complexes to CD14 [Ｊ]. J Immunol, 1999; 162(12)∶7454.
8. Lukkari TA, Jarvelainen HA, Oinonen T, et al. Shortterm ethanol exposure increases the expression of Kupffer cell CD14 receptor and lipopolysaccharide binding protein in rat liver [Ｊ]. Alcohol, 1999; 34(3)∶311.
9. Scott MG, Vreugdenhil AC, Buurman WA, et al. Cutting edge: cationic antimicrobial peptides block the binding of lipopolysaccharide (LPS) to LPS binding protein [Ｊ]. J Immunol, 2000; 164(2)∶549.
10. Amura CR, Kamel T, Ito N, et al. Differential regulation of lipopolysaccharide (LPS) activation pathways in mouse macrophages by LPSbinding proteins [Ｊ]. J Immunol, 1998; 161(5)∶2552.
11. Kitchens RL, Wolfbaue G, Albers JJ, et al. Plasm lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface [Ｊ]. J Biol Chem, 1999; 274(48)∶34116.
  1. 1. Nanbo A, Nishimura H, Muta T, et al. Lipopolysaccharide stimulates HepG2 human hepatoma cells in the presence of lipopolysaccharidebinding protein via CD14 [Ｊ]. Eur J Biochem,1999; 260(1)∶183.
  2. 2. Heumann D, Adachi Y, Le Roy D, et al. Role of plasma, lipopolysaccharidebinding protein, and CD14 in response of mouse peritoneal exudate macrophages to endotoxin [Ｊ]. Infect Immun, 2001; 69(1)∶378.
  3. 3. Gong JP, Wu CX, Liu CA,et al. Intestinal damage mediated by Kupffer cells in rats with endotoxemia [Ｊ]. World J Gastroenterol， 2002; 8(5)∶923.
  4. 4. Vreugdenhil AC, Dentener MA, Snoek AM, et al. Lipopolysaccharide binding protein and serum amyloid A secretion by human intestinal cells during the acute phase response [Ｊ]. J Immunol,1999; 163(5)∶2792.
  5. 5. Erwin PJ, Lewis H, Dolan S, et al. Lipopolysaccharide binding protein in acute pancreatitis [Ｊ]. Crit Care Med, 2000; 28(1)∶104.
  6. 6. Clark JG, Madtes DK, Martin TR, et al. Idiopathic pneumonia after bone marrow transplantation: cytokine activation and lipopolysaccharide amplification in the bronchoalveolar compartment [Ｊ]. Crit Care Med,1999; 27(9)∶1800.
  7. 7. Le Roy D, Di Padova F, Tees R, et al. Monoclonal antibodies to murine lipopolysaccharide (LPS)binding protein (LBP) protect mice from lethal endotoxemia by blocking either the binding of LPS to LBP or the presentation of LPS/LBP complexes to CD14 [Ｊ]. J Immunol, 1999; 162(12)∶7454.
  8. 8. Lukkari TA, Jarvelainen HA, Oinonen T, et al. Shortterm ethanol exposure increases the expression of Kupffer cell CD14 receptor and lipopolysaccharide binding protein in rat liver [Ｊ]. Alcohol, 1999; 34(3)∶311.
  9. 9. Scott MG, Vreugdenhil AC, Buurman WA, et al. Cutting edge: cationic antimicrobial peptides block the binding of lipopolysaccharide (LPS) to LPS binding protein [Ｊ]. J Immunol, 2000; 164(2)∶549.
  10. 10. Amura CR, Kamel T, Ito N, et al. Differential regulation of lipopolysaccharide (LPS) activation pathways in mouse macrophages by LPSbinding proteins [Ｊ]. J Immunol, 1998; 161(5)∶2552.
  11. 11. Kitchens RL, Wolfbaue G, Albers JJ, et al. Plasm lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface [Ｊ]. J Biol Chem, 1999; 274(48)∶34116.