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Abstract
Objective: Myocarditis is a serious disease, however no effective treatment exists. Plasminogen activator inhibitor-1 (PAI-1) is critical in cell recruitment and inflammation. Although inflammation is an essential pathological feature of acute myocarditis, the effects of PAI-1 inhibition on the development of acute myocarditis have not been well studied. Methods: To clarify the role of PAI-1, we used a rat experimental autoimmune myocarditis (EAM) model. Lewis rats were immunized on day 0 with porcine cardiac myosin to establish EAM. The rats with induced EAM were treated with the PAI-1 inhibitor (IMD-1622) (n = 8) or not treated (n = 6); hearts were harvested on day 21. Echocardiograms, heart weight to body weight ratios (H:B), histological examinations and in vitro studies were performed. Results: Echocardiograms indicated that the PAI-1 inhibitor improved left ventricular fractional shortening (50 ± 3%) compared with controls (36 ± 4%, p < 0.05). The inhibitor significantly reduced H:B ratios compared with controls. Pathologically, areas of myocardial cell infiltration and fibrosis in the inhibitor-treated group were significantly smaller than those in the control group. Immunohistochemistry revealed enhanced expression of adhesion molecules and inflammatory factors in non-treated EAM hearts, the inhibitor suppressed this expression. Conclusions: The PAI-1 inhibitor suppressed EAM development; thus this inhibitor is promising for treating clinical myocarditis.
Acknowledgments
We would like to thank Ms Noriko Tamura for excellent technical assistance.