Resveratrol attenuates lipopolysaccharide-induced hepatitis in D-galactosamine sensitized rats: role of nitric oxide synthase 2 and heme oxygenase-1
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19796704
DOI
10.1016/j.niox.2009.09.004
PII: S1089-8603(09)00119-0
Knihovny.cz E-resources
- MeSH
- Antioxidants pharmacology MeSH
- Cytoprotection * MeSH
- Galactosamine toxicity MeSH
- Heme Oxygenase (Decyclizing) genetics metabolism MeSH
- Liver drug effects enzymology pathology MeSH
- Rats MeSH
- Chemical and Drug Induced Liver Injury pathology prevention & control MeSH
- Lipopolysaccharides toxicity MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- Rats, Wistar MeSH
- Resveratrol MeSH
- Liver Failure chemically induced prevention & control MeSH
- Stilbenes pharmacology MeSH
- Nitric Oxide Synthase Type II genetics metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- Galactosamine MeSH
- Heme Oxygenase (Decyclizing) MeSH
- Hmox1 protein, rat MeSH Browser
- Lipopolysaccharides MeSH
- Nos2 protein, rat MeSH Browser
- Resveratrol MeSH
- Stilbenes MeSH
- Nitric Oxide Synthase Type II MeSH
The goal of study was directed to investigate the effects of resveratrol (RES) pretreatment on the enhancing action of D-galactosamine (D-GalN; 800 mg/kg) on lipopolysaccharide (LPS; 0.5 microg/kg) inducing liver failure in rats. Liver function was assessed by determination of plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), alpha-glutathione S-transferase (alpha GST) and bilirubin (BILI). Plasma NO(2)(-) was assessed by NO(2)(-)/NO(3)(-) colorimetric kit. The estimation of nonenzymatic and enzymatic antioxidants (glutathione and catalase) was performed in plasma and liver homogenate. Lipid peroxidation was evaluated by the thiobarbituric acid reacting substances (TBARS) and the conjugated dienes (CD). Morphological examinations using light and electron microscopy were performed. Observations related to pharmacological increases of inducible nitric oxide synthase (NOS-2)/nitric oxide (NO) and inducible heme oxygenase (HO-1) in fulminant hepatic failure and modulation by resveratrol were followed up by real-time reverse transcription PCR (RT-PCR) in liver tissue. In the present study we found that among the mechanisms responsible for the hepatoprotective effect of resveratrol in the LPS/D-GalN liver toxicity model are reduction in NO, downregulation of NOS-2, modification of oxidative stress parameters and modulation of HO-1 which led to overall improvement in hepatotoxic markers and morphology after the hepatic insult.
References provided by Crossref.org
SIRT1 Modulators in Experimentally Induced Liver Injury