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Título: | Metformin protects rat hepatocytes against bile acid-induced apoptosis |
Autor: | Woudenberg-Vrenken, Titia E.; Conde de la Rosa, Laura CSIC ORCID ; Buist-Homan, Manon; Faber, Klaas Nico; Moshage, Han | Fecha de publicación: | 2013 | Editor: | Public Library of Science | Citación: | PLoS ONE 8(8): e71773 (2013) | Resumen: | [Background]: Metformin is used in the treatment of Diabetes Mellitus type II and improves liver function in patients with non-alcoholic fatty liver disease (NAFLD). Metformin activates AMP-activated protein kinase (AMPK), the cellular energy sensor that is sensitive to changes in the AMP/ATP-ratio. AMPK is an inhibitor of mammalian target of rapamycin (mTOR). Both AMPK and mTOR are able to modulate cell death. [Aim]: To evaluate the effects of metformin on hepatocyte cell death. [Methods]: Apoptotic cell death was induced in primary rat hepatocytes using either the bile acid glycochenodeoxycholic acid (GCDCA) or TNFα in combination with actinomycin D (actD). AMPK, mTOR and phosphoinositide-3 kinase (PI3K)/Akt were inhibited using pharmacological inhibitors. Apoptosis and necrosis were quantified by caspase activation, acridine orange staining and Sytox green staining respectively. [Results]: Metformin dose-dependently reduces GCDCA-induced apoptosis, even when added 2 hours after GCDCA, without increasing necrotic cell death. Metformin does not protect against TNFα/ActD-induced apoptosis. The protective effect of metformin is dependent on an intact PI3-kinase/Akt pathway, but does not require AMPK/mTOR-signaling. Metformin does not inhibit NF-κB activation. [Conclusion]: Metformin protects against bile acid-induced apoptosis and could be considered in the treatment of chronic liver diseases accompanied by inflammation. © 2013 Woudenberg-Vrenken et al. | Descripción: | This is an open-access article distributed under the terms of the Creative Commons Attribution License. | Versión del editor: | http://dx.doi.org/10.1371/journal.pone.0071773 | URI: | http://hdl.handle.net/10261/88549 | DOI: | 10.1371/journal.pone.0071773 | Identificadores: | doi: 10.1371/journal.pone.0071773 e-issn: 1932-6203 |
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