Abstract
BackgroundWe showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus.MethodsFour-week-old inbred male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units (pfu) of the EMC virus. Cetirizine was administered orally at a dose of 1 or 10 mg/kg per day for the survival study, and 1 mg/kg for the histologic and gene expression studies, beginning on the day of viral inoculation.ResultsCetirizine improved survival dose dependently. Heart weight to body weight ratio was significantly decreased in mice treated with cetirizine. The area of myocardial necrosis was significantly smaller in the hearts of mice treated with cetirizine compared with controls. Gene expressions of tumor necrosis factor, interleukin 6, and metalloproteinase 2 were significantly suppressed in the hearts of mice treated with cetirizine.ConclusionThese results suggest that cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodeling in the hearts of mice.
Highlights
In recent years, mast cells have been implicated in the pathogenesis of cardiovascular and atherosclerotic disorders
We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice [3,4]
Cetirizine was dissolved in distilled water and given orally by gavage at a dose of 1 or 10 mg/kg per day starting on the same day on 1 or 10 mg/kg per day starting on the third day as the EMC virus inoculation
Summary
Mast cells have been implicated in the pathogenesis of cardiovascular and atherosclerotic disorders. Myocardial histamine and tryptase content, and mast cell density are higher in heart failure due to idiopathic dilated or ischemic cardiomyopathy than in control hearts [2]. Mast cell deficient mice developed less pronounced myocardial necrosis and cellular infiltration induced by encephalomyocarditis virus, and the histamine H1-receptor antagonist improved survival of mice and in improved histological changes [4]. We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. We investigated the effect of cetirizine, a selective H1 receptor antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus
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