脂多糖诱导小鼠脏器中胞间粘附分子-1的表达

Expression of intercellular adhesion molecule-1 in different organs of the mice with endotoxic shock induced by lipopolysaccharide

为研究脂多糖 (lipopolysaccharide,LPS)诱导的内毒素休克小鼠多种脏器中胞间粘附分子 1(intercellularadhesionmolecule 1,ICAM 1)表达的差异 ,用 5mg/kgLPS腹腔注射小鼠后 ,分别采用Westernblotting和RT PCR法检测组织中ICAM 1蛋白和mRNA的表达情况。结果显示 ,在正常小鼠 ,ICAM 1蛋白和mRNA的表达在肺中最多 ,其次是脾脏 ,在肾脏和肠有少量表达 ,在肝脏和心脏中未能检出。LPS腹腔注射后 6h可诱导小鼠发生内毒素休克 ,此时 ,ICAM 1蛋白表达仍以在肺中最多 ,在肝、脾、心、肾和肠依次减少 ;其中在肺、肾和脾分别比正常时增加 4 5、3 0和 1 5倍 ,而且在正常时不能检出的肝和心中呈现阳性 ,但在肠中则变化不大。脏器中ICAM 1mRNA亦相应显著增加。上述结果表明 ,在LPS诱导的内毒素休克小鼠的多种脏器中ICAM 1蛋白和mRNA表达显著增加。脏器间ICAM 1表达上调的差异可能带来内毒素休克时脏器的不同易伤性 ,抑制ICAM 1的表达可能对内毒素休克的防治有重要的意义。

To investigate and compare the expression of intercellular adhesion molecule 1 (ICAM 1) in different organs of the mice with endotoxic shock induced by lipopolysaccharide (LPS), protein and mRNA of ICAM 1 were measured by Western blotting and RT PCR respectively in different organs of BALB/c mice administered intraperitoneally with 5 mg/kg LPS The results showed that the constitutive expression of ICAM 1 protein and mRNA was the greatest in the lungs, followed by the spleen, kidney and intestine After LPS stimulation, the upregulation of ICAM 1 was still greatest in the lungs, followed by the liver, spleen, heart, kidney and intestine Compared with the normal mice, the expression of ICAM 1 protein in endotoxic shocked mice increased by 4 5 fold in the lungs, 3 0 fold in the kidney, 1 5 fold in the spleen; the expression in the liver and heart was negative under normal condition and changed into positive during endotoxic shock; but ICAM 1 expression in the intestine did not change significantly The expression of ICAM 1 mRNA also increased consistently These data highlight that LPS can up re gulate ICAM 1 protein and mRNA expression indifferent tissues of the mice with endotoxic shock.The difference in ICAM 1 expression among the organs may lead to different sensitivity of organ damage in endotoxic shock This suggests that inhibition of ICAM 1 expression may be a useful principle for prevention and treatment of endotoxic shock