OBJECTIVES: To investigate the effect of rosiglitazone, a synthetic selective peroxisome proliferator-activated receptor (PPAR)-gamma agonist, for cytokine production and PPAR-gamma expression in nasal mucosa. METHODS: Mice in allergic rhinitis group received ovalbumin sensitization followed by ovalbumin intranasal challenge. Mice in the rosiglitazone group received rosiglitazone treatment additionally. Various allergic responses were then assessed. RESULTS: The frequency of nasal rubs and ovalbumin-specific immunoglobulin E decreased significantly in the rosiglitazone group compared with the allergic rhinitis group. The rosiglitazone group also showed that inflammation was markedly reduced by rosiglitazone administration. Immunohistochemistry showed that PPAR-gamma protein expression in nasal mucosa was enhanced in the allergic rhinitis group and the rosiglitazone group compared with control mice. CONCLUSION: PPAR-gamma activation with rosiglitazone effectively inhibited allergic symptom development, nasal mucosal inflammation, and production of ovoalbumin-specific immunoglobulin E and Th2-type cytokine. Our results provide evidence of the therapeutic potential of PPAR-gamma agonist for the treatment of allergic rhinitis.
OBJECTIVES: To investigate the effect of rosiglitazone, a synthetic selective peroxisome proliferator-activated receptor (PPAR)-gamma agonist, for cytokine production and PPAR-gamma expression in nasal mucosa. METHODS:Mice in allergic rhinitis group received ovalbumin sensitization followed by ovalbumin intranasal challenge. Mice in the rosiglitazone group received rosiglitazone treatment additionally. Various allergic responses were then assessed. RESULTS: The frequency of nasal rubs and ovalbumin-specific immunoglobulin E decreased significantly in the rosiglitazone group compared with the allergic rhinitis group. The rosiglitazone group also showed that inflammation was markedly reduced by rosiglitazone administration. Immunohistochemistry showed that PPAR-gamma protein expression in nasal mucosa was enhanced in the allergic rhinitis group and the rosiglitazone group compared with control mice. CONCLUSION:PPAR-gamma activation with rosiglitazone effectively inhibited allergic symptom development, nasal mucosal inflammation, and production of ovoalbumin-specific immunoglobulin E and Th2-type cytokine. Our results provide evidence of the therapeutic potential of PPAR-gamma agonist for the treatment of allergic rhinitis.