Protective effect of recombinant TM-N and recombinant soluble RAGE in a mouse model of acute hepatic failure.
- VernacularTitle:重组血栓调节蛋白N端结构域和可溶性晚期糖化终末产物受体对急性肝衰竭模型鼠的保护作用
- Author:
Shao-fang HUANG
1
;
Fei WU
;
Wei LIU
;
Yong-wen HE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Galactosamine; adverse effects; Interleukin-1beta; blood; Liver; metabolism; Liver Failure, Acute; chemically induced; prevention & control; Mice; Mice, Inbred Strains; Receptor for Advanced Glycation End Products; Receptors, Immunologic; metabolism; Recombinant Proteins; pharmacology; Thrombomodulin; metabolism; Tumor Necrosis Factor-alpha; blood
- From: Chinese Journal of Hepatology 2013;21(10):759-763
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the roles of N-terminal lectin-like domain of thrombomodulin (TM-N) and receptor for advanced glycation end products (RAGE) in acute hepatic failure using a mouse model system.
METHODSAcute hepatic failure was induced in Kunming mice by intraperitoneal injection of D-galactosamine (D-Galn at 600 mg/kg) and lipopolysaccharide (LPS at 5 mug/kg) and mice were divided into groups for injection with saline, recombinant (r)TM-N protein, or recombinant soluble (rs)RAGE protein. Unmanipulated model mice served as the negative controls. Effects on liver expression of high mobility group box-1 (HMGB1) were detected by immunohistochemistry and real time RT-PCR. Effects on serum levels of tumor necrosis factor-alpha (TNFa) and interleukin-1 beta (IL)-1b were quantified by ELISA.
RESULTSTreatment with rTM-N and rsRAGE both alleviated the acute liver damage induced by D-Galn/LPS exposure, and decreased the hepatic expression of HMGB1 as well as the serum levels of TNFa and IL-1b.
CONCLUSIONIntraperitoneal delivery of rTM-N and rsRAGE can alleviate acute liver damage by modulating the expression of necrosis- and inflammation-related factors.
