脂多糖诱导小鼠脏器中胞间粘附分子-1的表达

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（intercellu-lar adhesion molecule-1,ICAM-1)表达的差异。用5mg/kgLPS腹腔注射小鼠后,分别采用Western blotting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。

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

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