Cited by 295Cardiac Ischemia and ReperfusionPeroxisome Proliferator-Activated ReceptorsCardiac Fibrosis and Remodeling

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In Vivo Myocardial Protection From Ischemia/Reperfusion Injury by the Peroxisome Proliferator–Activated Receptor-γ Agonist Rosiglitazone

Yue, Tian-li, Chen, Jun, Bao, Weike, Narayanan, Padma K., Bril, Antoine, Jiang, Wen, Lysko, Paul G., Gu, Juan-Li, Boyce, Rogely, Zimmerman, Dawn M., Hart, Timothy K., Buckingham, Robin E., Ohlstein, Eliot H.·2001·Circulation

DOI 10.1161/hc4601.099403

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Abstract

BackgroundDiabetes is associated with increased risk of mortality as a consequence of acute myocardial infarction. This study determined whether rosiglitazone (ROSI) could reduce myocardial infarction after ischemia/reperfusion injury. Methods and ResultsMale Lewis rats were anesthetized, and the left anterior descending coronary artery was ligated for 30 minutes. After reperfusion for 24 hours, the ischemic and infarct sizes were determined. ROSI at 1 and 3 mg/kg IV reduced infarct size by 30% and 37%, respectively (P<0.01 versus vehicle). Pretreatment with ROSI (3 mg · kg−1· d−1 PO) for 7 days also reduced infarct size by 24% (P<0.01). ROSI also improved ischemia/reperfusion-induced myocardial contractile dysfunction. Left ventricular systolic pressure and positive and negative maximal values of the first derivative of left ventricular pressure (dP/dt) were significantly improved in ROSI-treated rats. ROSI reduced the accumulation of neutrophils and macrophages in the ischemic heart by 40% and 43%, respectively (P<0.01). Ischemia/reperfusion induced upregulation of CD11b/CD18 and downregulation of L-selectin on neutrophils and monocytes; these effects were significantly attenuated in ROSI-treated animals. Likewise, intercellular adhesion molecule-1 expression in ischemic hearts was markedly diminished by ROSI, as was the ischemia/reperfusion-stimulated upregulation of monocyte chemoattractant protein-1. ConclusionsROSI reduced myocardial infarction and improved contractile dysfunction caused by ischemia/reperfusion injury. The cardioprotective effect of ROSI was most likely due to inhibition of the inflammatory response.

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10.1161/circ.102.11.1315 · DOI
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Authors: Yue, T.-L., Chen, J., Bao, W., Narayanan, P. K., Bril, A., Jiang, W., Lysko, P. G., Gu, J.-L., Boyce, R., Zimmerman, D. M., Hart, T. K., Buckingham, R. E., & Ohlstein, E. H.
Affiliations: From the Departments of Cardiovascular Pharmacology (T.Y., J.C., W.B., A.B., W.J., P.G.L., J.G., R.E.B., E.H.O.) and Safety Assessment (P.K.N., R.B., D.M.Z., T.K.H.), GlaxoSmithKline Pharmaceuticals, King of Prussia, Pa.
GlaxoSmithKline (United States) (US)
GlaxoSmithKline (United Kingdom) (GB)
ORCID: Bao, Weike
Bril, Antoine
Jiang, Wen
Boyce, Rogely
Zimmerman, Dawn M.
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2001-11-20
Volume: 104
Issue: 21
Pages: 2588-2594
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/hc4601.099403
OpenAlex: W2102772338
Cited by: 295
References: 32
Citations by year: 2026: 2 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 3 · 2021: 3 · 2020: 6 · 2018: 5 · 2017: 5 · 2016: 4 · 2015: 9 · 2014: 9 · 2013: 11 · 2012: 14
FWCI: 17.41
Type: journal article
Language: en
Open access: closed
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords: rosiglitazone, PPARγ agonists, myocardial ischemia-reperfusion injury, myocardial infarction, cardioprotection, infarct size, myocardial contractile dysfunction, neutrophil accumulation, macrophage accumulation, leukocyte adhesion molecules, CD11b/CD18, L-selectin, ICAM-1, MCP-1, inflammation, diabetes mellitus, acute myocardial infarction
MeSH terms: Rosiglitazone, Animals, Hypoglycemic Agents, Macrophages, Male, Monocytes, Myocardial Contraction, Myocardial Infarction, Neutrophils, Rats, Inbred Lew, RNA, Messenger, Thiazoles, Transcription Factors, Myocardial Reperfusion Injury, Cell Adhesion Molecules, Macrophage-1 Antigen, Receptors, Cytoplasmic and Nuclear, CD18 Antigens, Chemokine CCL2, Neutrophil Infiltration, Thiazolidinediones, Diabetes Complications, Rats

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In Vivo Myocardial Protection From Ischemia/Reperfusion Injury by the Peroxisome Proliferator–Activated Receptor-γ Agonist Rosiglitazone

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