Fenofibrate, a Peroxisome Proliferator-Activated Receptor α Activator, Suppresses Experimental Autoimmune Myocarditis by Stimulating the Interleukin-10 Pathway in Rats

• Maruyama Seitaro

  First Department of Internal Medicine, Niigata University School of Medicine

• Kato Kiminori

  First Department of Internal Medicine, Niigata University School of Medicine

• Kodama Makoto

  First Department of Internal Medicine, Niigata University School of Medicine

• Hirono Satoru

  First Department of Internal Medicine, Niigata University School of Medicine

• Fuse Koichi

  First Department of Internal Medicine, Niigata University School of Medicine

• Nakagawa Osamu

  First Department of Internal Medicine, Niigata University School of Medicine

• Nakazawa Mikio

  Department of Pharmacology, Niigata University School of Medicine

• Miida Takashi

  Department of Laboratory Medicine, Niigata University School of Medicine

• Yamamoto Tadashi

  Department of Pathology, Institute of Nephrology, Niigata University School of Medicine

• Watanabe Kenichi

  Department of Clinical Parmacology, Niigata College of Pharmacy

• Aizawa Yoshifusa

  First Department of Internal Medicine, Niigata University School of Medicine

Bibliographic Information

Other Title

• Fenofibrate, a Peroxisome Proliferator-Activated Receptor α Activator, Suppresses Experimental Autoimmune Myocarditis by Stimulating the Interleukin-10 Pathway in Rats

Abstract

Experimental autoimmune myocarditis (EAM) in rats is an animal model of human giant cell myocarditis and postmyocarditis dilated cardiomyopathy. As the heart consumes large amounts of energy, heart diseases such as myocarditis and dilated cardiomyopathy are associated with abnormal fatty acid metabolism. Peroxisome proliferator-activated receptor α (PPARα) is a regulator of the oxidative degradation of fatty acids. To investigate the role of PPARα in EAM, fenofibrate (a PPARα activator) was administered to rats with EAM for 4 weeks. Reductions in the ratios of both ventricular weight to body weight and the area of inflammatory lesions to the total area of heart sections were observed in fenofibrate-treated rats when compared with controls. Fenofibrate ameliorated changes in serum albumin and sialic acid, which are markers of inflammation. Cardiac expression of interleukin-10 (IL-10) mRNA was more pronounced in the fenofibrate group than in the control group (1.3±0.2 vs 0.7±0.1; p<0.01), and the area of intact myocardium correlated with the IL-10 mRNA level (p=0.0297, r=0.620). We suggest that PPARα activators may prevent the progression of myocarditis through increased expression of the gene encoding the anti-inflammatory cytokine IL-10, although the mechanisms involved remain to be determined.

Journal

• Journal of Atherosclerosis and Thrombosis

  Journal of Atherosclerosis and Thrombosis 9 (2), 87-92, 2002

  Japan Atherosclerosis Society

Keywords

• Experimental autoimmune myocarditis
• Fenofibrate
• Peroxisome proliferator-activated receptor α
• Interleukin-10

Details

• CRID: 1390282679409019904
• NII Article ID: 10010270394
• NII Book ID: AA11018976
• DOI: 10.5551/jat.9.87
• ISSN: 18803873
• ISSN: 13403478
• PubMed: 12236317
• Web Site: https://www.jstage.jst.go.jp/article/jat/9/2/9_2_87/_pdf
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• Abstract License Flag: Disallowed