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Tytuł pozycji:

Ezetimibe Prevents Ischemia/Reperfusion-Induced Oxidative Stress and Up-Regulates Nrf2/ARE and UPR Signaling Pathways.

Tytuł:
Ezetimibe Prevents Ischemia/Reperfusion-Induced Oxidative Stress and Up-Regulates Nrf2/ARE and UPR Signaling Pathways.
Autorzy:
Peserico D; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Stranieri C; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Garbin U; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Mozzini C C; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Danese E; Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.
Cominacini L; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Fratta Pasini AM; Department of Medicine, Section of General Medicine and Atherothrombotic and Degenerative Diseases, University of Verona, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy.
Źródło:
Antioxidants (Basel, Switzerland) [Antioxidants (Basel)] 2020 Apr 23; Vol. 9 (4). Date of Electronic Publication: 2020 Apr 23.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI AG, [2012]-
References:
Annu Rev Pharmacol Toxicol. 2007;47:89-116. (PMID: 16968214)
Nat Rev Mol Cell Biol. 2012 Jan 18;13(2):89-102. (PMID: 22251901)
Nat Cell Biol. 2010 Mar;12(3):213-23. (PMID: 20173742)
Free Radic Biol Med. 2014 Mar;68:178-85. (PMID: 24373961)
Circulation. 2010 Jul 6;122(1):11-9. (PMID: 20566952)
Biochim Biophys Acta Mol Basis Dis. 2017 Feb;1863(2):585-597. (PMID: 27825853)
Mol Med Rep. 2018 Jul;18(1):675-683. (PMID: 29845269)
PLoS One. 2009 Dec 09;4(12):e8225. (PMID: 20011043)
Int J Biol Macromol. 2019 Mar 15;125:496-502. (PMID: 30468811)
Free Radic Res. 2015;49(8):927-34. (PMID: 25744598)
Free Radic Biol Med. 2018 Mar;117:76-89. (PMID: 29373843)
J Biol Chem. 2004 May 7;279(19):20108-17. (PMID: 14978030)
Arterioscler Thromb Vasc Biol. 2007 Sep;27(9):1991-7. (PMID: 17600225)
Nat Med. 2011 Nov 07;17(11):1391-401. (PMID: 22064429)
Toxicol Lett. 2015 Oct 14;238(2):83-9. (PMID: 26220517)
Circ Res. 2006 May 12;98(9):1186-93. (PMID: 16601230)
Free Radic Res. 2015 Mar;49(3):244-52. (PMID: 25511473)
Biochem Pharmacol. 2000 Oct 15;60(8):1075-83. (PMID: 11007944)
Expert Opin Pharmacother. 2005 Jan;6(1):131-9. (PMID: 15709890)
Clin Pharmacokinet. 2005;44(5):467-94. (PMID: 15871634)
Cell Metab. 2012 Mar 7;15(3):361-71. (PMID: 22405071)
Exp Neurol. 2018 Sep;307:12-23. (PMID: 29852178)
J Atheroscler Thromb. 2018 Sep 1;25(9):808-820. (PMID: 29540636)
Mol Cell. 2013 Feb 7;49(3):379-87. (PMID: 23395268)
Physiol Rev. 2008 Apr;88(2):581-609. (PMID: 18391174)
Annu Rev Physiol. 2011;73:239-59. (PMID: 20809793)
J Exp Med. 2017 Feb;214(2):423-437. (PMID: 28082356)
Genes Cells. 2011 Feb;16(2):123-40. (PMID: 21251164)
Biochim Biophys Acta. 2014 Sep;1842(9):1638-47. (PMID: 24915518)
Nat Rev Cardiol. 2016 Apr;13(4):193-209. (PMID: 26843289)
Am J Physiol Endocrinol Metab. 2009 Nov;297(5):E1030-8. (PMID: 19654286)
J Biol Chem. 2010 Jul 16;285(29):22576-91. (PMID: 20452972)
Atherosclerosis. 2016 Apr;247:40-7. (PMID: 26868507)
Free Radic Biol Med. 2016 Oct;99:520-532. (PMID: 27634173)
J Biol Chem. 2009 Oct 23;284(43):29735-45. (PMID: 19622751)
N Engl J Med. 2007 Sep 13;357(11):1121-35. (PMID: 17855673)
PLoS One. 2016 Sep 16;11(9):e0163046. (PMID: 27636901)
Oxid Med Cell Longev. 2020 Jan 4;2020:4717258. (PMID: 31998437)
Arch Med Sci. 2014 Aug 29;10(4):817-24. (PMID: 25276169)
Contributed Indexing:
Keywords: ER stress; Ezetimibe; Nrf2; ischemia-reperfusion; oxidative stress
Entry Date(s):
Date Created: 20200429 Latest Revision: 20200928
Update Code:
20240105
PubMed Central ID:
PMC7222361
DOI:
10.3390/antiox9040349
PMID:
32340270
Czasopismo naukowe
Background: While reperfusion is crucial for survival after an episode of ischemia, it also causes oxidative stress. Nuclear factor-E2-related factor 2 (Nrf2) and unfolded protein response (UPR) are protective against oxidative stress and endoplasmic reticulum (ER) stress. Ezetimibe, a cholesterol absorption inhibitor, has been shown to activate the AMP-activated protein kinase (AMPK)/Nrf2 pathway. In this study we evaluated whether Ezetimibe affects oxidative stress and Nrf2 and UPR gene expression in cellular models of ischemia-reperfusion (IR).
Methods: Cultured cells were subjected to simulated IR with or without Ezetimibe.
Results: IR significantly increased reactive oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP). Ezetimibe significantly decreased the cellular ROS formation and apoptosis induced by IR. These effects were paralleled by the up-regulation of Nrf2/ARE and ATF6 gene expression and by a down-regulation of CHOP. We also found that Nrf2 activation was dependent on AMPK, since Compound C, a pan inhibitor of p-AMPK, blunted the activation of Nrf2.
Conclusions: Ezetimibe counteracts IR-induced oxidative stress and induces Nrf2 and UPR pathway activation.

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