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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, RESULTS. Meshes: Animals, Autoimmune Diseases, Cells, Cultured, Dose-Response Relationship, Drug, Ligands, Myocarditis, Myocytes, Cardiac, Pioglitazone, Prostaglandin D2, Rats, Rats, Inbred Lew, Receptors, Cytoplasmic and Nuclear, Swine, T-Lymphocytes, Thiazolidinediones, Transcription Factors.
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Do peroxisome proliferator-activated receptor-gamma ligands ameliorate experimental autoimmune myocarditis associated with inhibition of self-sensitive T cells? Context: Recent evidence has suggested that peroxisome proliferator-activated receptor-gamma (PPAR-gamma) serves as a negative regulator in the immune system. In the present study, we investigated the expression of PPAR-gamma and the effect of PPAR-gamma ligands on experimental autoimmune myocarditis (EAM). Experimental autoimmune myocarditis was induced in Lewis rats by immunization with porcine cardiac myosin. PPAR-gamma ligands 15-deoxy-Delta-PGJ2 200 microg x kg(-1) x d(-1) by ip and pioglitazone 10 mg x kg(-1) x d(-1) by oral were administered for 3 weeks. PPAR-gamma expression was upregulated in myocarditis and the enhanced PPAR-gamma expression was prominently stained in the nuclear and perinuclear regions of the positive-stained cells in the inflammatory lesions. Administration of PPAR-gamma ligands markedly reduced the severity of myocarditis, as indicated by the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores, and microscopic scores. The upregulated PPAR-gamma expression was also reduced by PPAR-gamma ligands treatment. In addition, PPAR-gamma ligands suppressed the proliferative response and interferon-gamma production of T cell-enriched splenocytes from rats with EAM. Furthermore, the cytotoxic activity and myocarditogenic potential of these T cells were inhibited by PPAR-gamma ligands treatment.
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PPAR-gamma ligands ameliorate EAM associated with inhibition of expansion and activation of the self-sensitive T cells. These results suggest that PPAR-gamma ligands may have the potential to modulate human inflammatory heart diseases as myocarditis. Final Decision: yes