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• W2981672502 abstract "Abstract Purpose Myocarditis and dilated cardiomyopathy represent the acute and chronic phases of an inflammatory disease of the myocardium, for which no standardized treatment is currently available in clinical practice. Myocardial fibrosis an oxidative stress are pathogenic factors associated with these processes. However, new research has found that gut health can be linked to some cardiac conditions. Thus, in this study we investigated whether intestinal disturbances are present in myocarditis, using a murine experimental autoimmune model (EAM) that mimics human myocarditis, as well as the potential beneficial effect of treatment with the mitochondrial antioxidant, MitoQ. Methods and results EAM was induced in BALB/c mice with a myocardiogenic peptide and mice were treated with MitoQ (50 mg/kg/day, i.p). On day 21 (acute phase), we assessed signs of heart injury (e.g. hypertrophy, fibrosis, oxidative stress) and parameters related to gut damage such as accumulation of reactive oxigen species (superoxide anion: O2·−), inflammation (IL-1β, IL-33, TNFα), microbial translocation (sCD14; intestinal fatty acid binding protein, I-FABP) and mucins in serum and/or intestine. MitoQ teatment significantly reduced the high heart weight/body weight ratio (HW/BW) of EAM mice, a characteristic hallmark of cardiac hyperthropy. Histological analysis of hearts showed presence of fibrosis (Sirius Red stain) and high O2·− levels (DHE stain) in EAM mice whereas these effects were not detectable in cardiac tissue from healthy or MitoQ-treated EAM mice. In addition, the enhanced O2·− ions (DHE stain) and mucin loss (Alcian Blu/PAS stain) found in colon, ileum, jejunum and duodenum sections from EAM mice were attenuated by MitoQ treatment. The systemic markers associated to intestinal barrier disruption, sCD14 and I-FABP, were found strongly increased in serum from EAM mice, and MitoQ prevents this rise. The beneficial MitoQ effects were also associated with a decrease in the pro-inflammatory cytokines TNFα, IL-33 and IL-1β, both in serum and colonic tissue of treated-EAM mice, as well as a reduction of the myeloperoxidase activity in colon, compared with untreated EAM mice. Conclusion Our data show that in addition to the heart, the intestinal tissue is also damaged in the preclinical model of experimental autoimmune myocarditis, and that MitoQ treatment could reverse this profile. Since there are systemic markers released from the intestine, therapeutic strategies targeting to prevent the intestinal oxidative stress and its associated gut barrier dysfunction, could contribute to the amelioration of the disease. Acknowledgement/Funding SAF2016-81063; CIBERCV" @default.
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• W2981672502 date "2019-10-01" @default.
• W2981672502 modified "2023-10-17" @default.
• W2981672502 title "P6284The antioxidant MitoQ protects against intestinal disturbances in the experimental autoimmune model of myocarditis" @default.
• W2981672502 doi "https://doi.org/10.1093/eurheartj/ehz746.0882" @default.
• W2981672502 hasPublicationYear "2019" @default.
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