脂多糖诱导小鼠脏器中胞间粘附分子-1的表达

 

 


闫文生1, 阚文宏1, 黄巧冰1, 姜勇1, 王士雯2, 赵克森1,*


(1
第一军医大学全军休克微循环重点实验室, 广州 510515; 
2
中国人民解放军总医院老年心血管病研究所, 北京 100853)

摘 要:
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-1intercellular adhesion molecule-1, ICAM-1)表达的差异, 5 mg/kg LPS腹腔注射小鼠后, 分别采用Western blotting RT-PCR法检测组织中ICAM-1蛋白和mRNA的表达情况。 结果显示, 在正常小鼠中, ICAM-1蛋白和mRNA的表达在肺中最多, 其次是脾, 在肾和肠有少量表达, 在肝和心中未能检出。LPS腹腔注射后6 h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4.53.01.5, 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-1 mRNA亦相应显著增加。上述结果表明, 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。

关键词:
内毒素休克
; 脂多糖胞间粘附分子-1
学科分类号:
R363R631.4

 

 

 

 

 

 

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

 

 


YAN Wen-Sheng1, KAN Wen-Hong1, HUANG Qiao-Bing1, JIANG Yong1, WANG Shi-Wen2, ZHAO Ke-Sen1,*
(1Key Laboratory of Shock and Microcirculation of PLA, The First Military Medical University, Guangzhou 510515;  2The Institute of Geriatric Cardiology, General Hospital of PLA, Beijing 100853)

Abstract: 
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-regulate ICAM
1 protein and mRNA expression in different tissues of the mice with endotoxic shock.The difference in ICAM1 expression among the organs may lead to different sensitivity of organ damage in endotoxic shock. This suggests that inhibition of ICAM1 expression may be a useful principle for prevention and treatment of endotoxic shock.

Key words:
endotoxic shock
lipopolysaccharideintercellular adhesion molecule1

 

 

 

 

 

 

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