Expression of intercellular adhesion molecule-1 in different organs of the mice with endotoxic shock induced by lipopolysaccharide.
- Author:
Wen-Sheng YAN
1
;
Wen-Hong KAN
;
Qiao-Bing HANG
;
Yong JIANG
;
Shi-Wen WANG
;
Ke-Sen ZHAO
Author Information
1. Key Laboratory of Shock and Microcirculation of PLA, The First Military Medical University, Guangzhou 510515.
- Publication Type:Journal Article
- MeSH:
Animals;
Intercellular Adhesion Molecule-1;
biosynthesis;
Kidney;
metabolism;
Lipopolysaccharides;
Lung;
metabolism;
Male;
Mice;
Mice, Inbred BALB C;
RNA, Messenger;
biosynthesis;
Shock, Septic;
chemically induced;
metabolism
- From:
Acta Physiologica Sinica
2002;54(1):71-74
- CountryChina
- Language:Chinese
-
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 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.
