Resveratrol attenuates lipopolysaccharide-induced hepatitis in D-galactosamine sensitized rats: role of nitric oxide synthase 2 and heme oxygenase-1
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
19796704
DOI
10.1016/j.niox.2009.09.004
PII: S1089-8603(09)00119-0
Knihovny.cz E-zdroje
- MeSH
- antioxidancia farmakologie MeSH
- cytoprotekce * MeSH
- galaktosamin toxicita MeSH
- hemová oxygenasa (decyklizující) genetika metabolismus MeSH
- játra účinky léků enzymologie patologie MeSH
- krysa rodu Rattus MeSH
- lékové postižení jater patologie prevence a kontrola MeSH
- lipopolysacharidy toxicita MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Wistar MeSH
- resveratrol MeSH
- selhání jater chemicky indukované prevence a kontrola MeSH
- stilbeny farmakologie MeSH
- synthasa oxidu dusnatého, typ II genetika metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antioxidancia MeSH
- galaktosamin MeSH
- hemová oxygenasa (decyklizující) MeSH
- Hmox1 protein, rat MeSH Prohlížeč
- lipopolysacharidy MeSH
- Nos2 protein, rat MeSH Prohlížeč
- resveratrol MeSH
- stilbeny MeSH
- synthasa oxidu dusnatého, typ 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.
Citace poskytuje Crossref.org
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