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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Autoimmune Diseases, Blotting, Western, Cell Nucleus, Cell Proliferation, Fatty Acids, Monounsaturated, Fluvastatin, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Indoles, Interferon-gamma, Interleukin-2, Lymphocyte Activation, Models, Animal, Myocarditis, Myocardium, Myosins, NF-kappa B, Rats, Rats, Inbred Lew, T-Lymphocytes.
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Does hMG-CoA reductase inhibitor attenuate experimental autoimmune myocarditis through inhibition of T cell activation? Context: This study tested the hypothesis that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor affects T cell-mediated autoimmunity through inhibition of nuclear factor-kappaB (NFkappaB) and reduces the severity of experimental autoimmune myocarditis (EAM). EAM was induced in Lewis rats by immunization with myosin. High-dose or low-dose fluvastatin or vehicle was administered orally for 3 weeks to rats with EAM. Fluvastatin reduced the pathophysiological severity of myocarditis. Fluvastatin inhibited expression of NFkappaB in the nuclei of myocardium in EAM. Fluvastatin reduced production of Th1-type cytokines, including interferon (IFN)-gamma and interleukin (IL)-2, and inhibited expression of inflammatory cytokine mRNAs in the myocardium. Infiltration of CD4-positive T cells into the myocardium and T cell proliferative responses were suppressed by fluvastatin. Plasma lipid levels did not differ between the groups.
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Fluvastatin ameliorates EAM by inhibiting T cell responses and suppressing Th1-type and inflammatory cytokines via inactivation of nuclear factor-kappaB, and this activity is independent of cholesterol reduction. Final Decision: yes