Protective action of ulinastatin against lipopolysaccharides-induced acute lung injury in mice and the relation of it to iNOS and c-Jun expressions.
- Author:
Zheng-huai TAN
1
;
Ling-hong YU
;
Huai-ling WEI
;
Geng-tao LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Glycoproteins; administration & dosage; pharmacology; Injections, Intraperitoneal; Lipopolysaccharides; Lung; drug effects; metabolism; pathology; Male; Mice; Mice, Inbred ICR; Nitric Oxide Synthase Type II; biosynthesis; genetics; Protective Agents; administration & dosage; pharmacology; Proto-Oncogene Proteins c-fos; biosynthesis; Proto-Oncogene Proteins c-jun; biosynthesis; RNA, Messenger; biosynthesis; genetics; Respiratory Distress Syndrome, Adult; chemically induced; metabolism; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha; biosynthesis; blood; genetics
- From: Acta Pharmaceutica Sinica 2006;41(7):636-640
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the protective action of ulinastatin against lipopolysaccharide (LPS)-induced acute lung injury in mice and the mechanism of its action.
METHODSMice were intraperitoneally injected with ulinastatin (50 and 100 ku x kg(-1)) or saline at a period of 12 h, separately, 30 min after the last injection of ulinastatin, except normal control, all mice of other groups were injected a dose of LPS 15 mg x kg(-1) via tail vein. The levels of TNFalpha in serum and lung were measured by ELISA. The expression of TNFalpha mRNA and iNOS mRNA in lung was assayed by RT-PCR. The expression of c-Fos and c-Jun protein in lung was measured by Western blotting method. And the NO2- / NO3- level in serum and MDA in lung were measured with kits.
RESULTSThe levels of NO2- / NO3- and TNFalpha in serum, MDA and TNFa in lung all increased after iv injection of LPS. The expressions of TNFa mRNA, iNOS mRNA, c-Fos and c-Jun in lung of LPS-injected mice were enhanced. Pretreatment with ulinastatin 100 ku x kg(-1) decreased the levels of NO2- / NO3- in serum and lung, reduced the index of lung, and inhibited the expressions of iNOS mRNA and c-Jun in lung induced by LPS in mice, while ulinastatin showed no effect on TNFa level in serum and lung.
CONCLUSIONUlinastatin protected mice from acute lung injury induced by lipopolysaccharides via inhibiting the activation of c-Jun and iNOS mRNA expression.
