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

目的探討內(nèi)毒素血癥時大鼠肝組織中脂多糖結合蛋白mRNA的表達、血漿中脂多糖結合蛋白(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)毒素血癥動物模型,檢測不同時點模型鼠肝組織中LBP mRNA的表達,同時檢測血漿中LBP、內(nèi)毒素、TNFα及IL6含量的變化,并與對照組相比較。另取肝組織在電鏡下觀察其病理學改變。結果隨著內(nèi)毒素血癥時間的延長,內(nèi)毒素組大鼠肝組織LBP mRNA的表達明顯增強,血漿中LBP、TNFα和IL6含量也明顯增加,與對照組比較差異有高度顯著性(P<0.01)。電鏡觀察見肝細胞脂肪變,線粒體空化,枯否氏細胞數(shù)量增多、體積增大、吞噬功能增強。結論內(nèi)毒素血癥時,大鼠肝組織中LBP mRNA表達明顯增強,血漿中LBP含量也明顯增加。由此提示,增高的LBP可能在脂多糖介導的枯否氏細胞激活及產(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,劉長安,李生偉. 內(nèi)毒素血癥時大鼠脂多糖結合蛋白的變化及其意義. 中國普外基礎與臨床雜志, 2003, 10(4): 355-358. doi: 復制

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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.
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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.