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Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation
M. Cahova, E. Palenickova, H. Dankova, E. Sticova, M. Burian, Z. Drahota, Z. Cervinkova, O. Kucera, C. Gladkova, P. Stopka, J. Krizova, Z. Papackova, O. Oliyarnyk, L. Kazdova,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26045616
DOI
10.1152/ajpgi.00329.2014
Knihovny.cz E-zdroje
- MeSH
- adenosintrifosfát metabolismus MeSH
- antiflogistika farmakologie MeSH
- antioxidancia farmakologie MeSH
- apoptóza účinky léků MeSH
- časové faktory MeSH
- cytoprotekce MeSH
- dieta s vysokým obsahem tuků MeSH
- energetický metabolismus účinky léků MeSH
- jaterní mitochondrie účinky léků metabolismus patologie MeSH
- játra účinky léků metabolismus patologie MeSH
- mediátory zánětu metabolismus MeSH
- metformin farmakologie MeSH
- modely nemocí na zvířatech MeSH
- nealkoholová steatóza jater farmakoterapie etiologie metabolismus patologie MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- reperfuzní poškození etiologie metabolismus patologie prevence a kontrola MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Nonalcoholic fatty liver disease is associated with chronic oxidative stress. In our study, we explored the antioxidant effect of antidiabetic metformin on chronic [high-fat diet (HFD)-induced] and acute oxidative stress induced by short-term warm partial ischemia-reperfusion (I/R) or on a combination of both in the liver. Wistar rats were fed a standard diet (SD) or HFD for 10 wk, half of them being administered metformin (150 mg·kg body wt(-1)·day(-1)). Metformin treatment prevented acute stress-induced necroinflammatory reaction, reduced alanine aminotransferase and aspartate aminotransferase serum activity, and diminished lipoperoxidation. The effect was more pronounced in the HFD than in the SD group. The metformin-treated groups exhibited less severe mitochondrial damage (markers: cytochrome c release, citrate synthase activity, mtDNA copy number, mitochondrial respiration) and apoptosis (caspase 9 and caspase 3 activation). Metformin-treated HFD-fed rats subjected to I/R exhibited increased antioxidant enzyme activity as well as attenuated mitochondrial respiratory capacity and ATP resynthesis. The exposure to I/R significantly increased NADH- and succinate-related reactive oxygen species (ROS) mitochondrial production in vitro. The effect of I/R was significantly alleviated by previous metformin treatment. Metformin downregulated the I/R-induced expression of proinflammatory (TNF-α, TLR4, IL-1β, Ccr2) and infiltrating monocyte (Ly6c) and macrophage (CD11b) markers. Our data indicate that metformin reduces mitochondrial performance but concomitantly protects the liver from I/R-induced injury. We propose that the beneficial effect of metformin action is based on a combination of three contributory mechanisms: increased antioxidant enzyme activity, lower mitochondrial ROS production, and reduction of postischemic inflammation.
Clinical and Transplant Pathology Department Charles University Prague Czech Republic
Department of Cell Biology Faculty of Science Charles University Prague Czech Republic
Department of Chemistry University of Cambridge Cambridge United Kingdom
Institute of Inorganic Chemistry Academy of Science CR Husinec Rez Czech Republic
Institute of Physiology Czech Academy of Sciences Prague Czech Republic
Citace poskytuje Crossref.org
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