ArticleLangenbeck's archives of surgery2010
Heme oxygenase (HO)-1 protects from lipopolysaccharide (LPS)-mediated liver injury by inhibition of hepatic leukocyte accumulation and improvement of microvascular perfusion.
Article in Langenbeck's archives of surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Efficacy of MK615 for the treatment of patients with liver disorders.World journal of gastroenterology · 2012Trial
- Pectolinarigenin Induces Antioxidant Enzymes through Nrf2/ARE Pathway in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Protective effect of ultrasonication-processed ginseng berry extract on the D-galactosamine/lipopolysaccharide-induced liver injury model in rats.Journal of ginseng research · 2018Article
- Beyond Preconditioning: Postconditioning as an Alternative Technique in the Prevention of Liver Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2016Review
- Intrahepatic microcirculatory disorder, parenchymal hypoxia and NOX4 upregulation result in zonal differences in hepatocyte apoptosis following lipopolysaccharide- and D-galactosamine-induced acute liver failure in rats.International journal of molecular medicine · 2014Article
- Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model.Journal of inflammation (London, England) · 2014Article
- LPS pretreatment ameliorates D-galactosamine/lipopolysaccharide-induced acute liver failure in rat.International journal of clinical and experimental pathology · 2014Article
- Direct in vivo observations of P-selectin glycoprotein ligand-1-mediated leukocyte-endothelial cell interactions in the pulmonary microvasculature in abdominal sepsis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
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4 authors at 1 institution in 1 country.
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Abstract
purposeLipopolysaccharide (LPS) represents a highly toxic substance which may aggravate morbidity and mortality in septic diseases. A recent study has reported that the induction of heme oxygenase (HO)-1 protects from LPS-induced liver injury. The mechanisms of action however, have not been clarified yet. Therefore, we analyzed in vivo the effects of HO-1 on the liver microcirculation under conditions of LPS exposure.
methodsIn C57BL/6 mice, endotoxemia was induced by intraperitoneal (i.p.) administration of LPS (500 microg/kg) and D-galactosamine (Gal, 800 mg/kg). HO-1 was induced in vivo by pretreatment with hemin dissolved in DMSO (50 micromol/kg i.p.). Animals treated with DMSO only served as controls. Six hours after LPS exposure the hepatic microcirculation and leukocyte-endothelial cell interaction were analyzed by intravital fluorescence microscopy. HO-1 expression was determined by Western blot analysis. Hepatocellular damage was assessed by measuring the serum levels of aspartate aminotransferase and alanine aminotransferase. In addition, leukocyte transmigration and hepatocellular apoptosis were analyzed by histology and immunohistochemistry.
resultsIn controls, LPS/Gal caused severe liver injury, as indicated by increased liver enzyme levels and apoptotic cell death. This was associated with distinct sinusoidal perfusion failure and microvascular intrahepatic leukocyte accumulation. Of interest, induction of HO-1 significantly reduced numbers of adherent and extravascular leukocytes when compared to controls. Moreover, microvascular perfusion was significantly improved, resulting in a decrease of AST and ALT and a reduction of hepatocellular apoptosis.
conclusionsOur novel data indicate that induction of HO-1 protects the liver from LPS-mediated injury by reducing leukocytic inflammation and improving intrahepatic microcirculation.
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