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Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation
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SYSNO ASEP 0448388 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation Tvůrce(i) Cahová, M. (CZ)
Páleníčková, E. (CZ)
Danková, H. (CZ)
Sticová, E. (CZ)
Burian, M. (CZ)
Drahota, Zdeněk (FGU-C) RID, ORCID
Červinková, Z. (CZ)
Kučera, O. (CZ)
Gladkova, Ch. (GB)
Stopka, Pavel (UACH-T) SAI
Křížová, Jana (UACH-T) SAI
Papáčková, Z. (CZ)
Oliyarnyk, O. (CZ)
Kazdová, L. (CZ)Zdroj.dok. American Journal of Physiology-Gastrointestinal and Liver Physiology. - : American Physiological Society - ISSN 0193-1857
Roč. 309, č. 2 (2015), G100-G111Poč.str. 12 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova metformin ; oxidative stress ; mitochondrial respiration ; liver injury ; 31P MR spectroscopy Vědní obor RIV EB - Genetika a molekulární biologie Vědní obor RIV – spolupráce Ústav anorganické chemie - Anorganická chemie CEP LL1204 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Institucionální podpora FGU-C - RVO:67985823 ; UACH-T - RVO:61388980 UT WOS 000357990800005 EID SCOPUS 84937398039 DOI 10.1152/ajpgi.00329.2014 Anotace 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. 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 and apoptosis. 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 mitochondrial ROS production in vitro. The effect of I/R was significantly alleviated by previous metformin treatment. Metformin downregulated the I/R-induced expression of proinflammatory and infiltrating monocyte and macrophage 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 Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2016
Počet záznamů: 1