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Updated: Aug 30, 2026
Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach
Published on: May 2, 2018
In vivo expression of lipopolysaccharide binding protein and its gene induced by endotoxin
Xu-hong Li1, Jian-ping Gong, Bing Tu
1Department of General Surgery, the Second College of Clinical Medicine, Chongqing 400010, China.
Objective:
To investigate the expression of lipopolysaccharide binding protein (LBP) and its gene in rats with endotoxemia and explore the role of LBP in the response of host to endotoxin.
Methods:
Thirty Wistar rats were divided randomly into five groups: the normal group and the endotoxemia groups (1, 3, 6, 12 hours after LPS injection, respectively). The level of plasma endotoxin was determined by the Limulus Amebocyte Lysate assay. The expression of LBP mRNA in hepatic tissue was examined by reverse transcription polymerase chain reaction (RT-PCR). Plasma levels of LBP, tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were measured by enzyme-linked immunosorbent assay (ELISA). Morphologic changes of hepatic tissue were observed under transmission electron microscope.
Results:
The level of plasma endotoxin peaked at 1 h after LPS injection, then declined, but was still higher than that of the normal group at 12 h; intrahepatic expression of LBP mRNA and plasma LBP increased with time after LPS stimulation; TNF-alpha and IL-6 in plasma increased with upregulation of LBP expression; there were significant differences between the normal group and endotoxemia groups (P<0.05). Activation of Kupffer cells and injury of hepatocytes could be seen in rats with endotoxemia.
Conclusions:
LPS can upregulate the intrahepatic expression of LBP mRNA and increase the plasma LBP level. Under certain conditions, LBP may enhance the sensitivity of host to the toxic effects of LPS.
