Effect of PPARγ on the airway vascular remodeling in the asthmatic mice

Objective To explore the effect of PPARγ on the airway vascular remodeling in the asthmatic mice.Methods A mouse model of asthma induced by sensitization and airway challenged with ovalbumin.Rosiglitazone (a PPARγ agonist),GW9662 (a PPARγ antagonist) and budesonide were administered by means of nebulization in rosiglitazone group (RG),GW9662 group (GG) and budesonide group (BG) respectively.The thickness of airway vascular wall and collagen deposition around airway vessels were measured and recorded,along with the parameters associated with airway inflammation (the cells count and the IL-4 level in the bronchoalveolar lavage fluid,and the inflammation cell score around the airway) and airway remodeling (the goblet cell hyperplasia in the lumens,thickness of airway smooth muscle and amount of collagen deposition around the bronchus).The expression of PPARγ was assaged by western blot.Results Above all assessed parameters were higher in AG than in CG,special for the thickness 0f airway vascular wall [(4.66±0.73) μm vs (2.87±0.46)μm] and collagen deposition around airway vessels [(22.1±2.42) μm~2/μm vs (1.73±0.73) μm~2/m],and were reduced by treatment of rosiglitazone [(3.95±0.90) and (9.97±1.56) μm~2/μm] or budesonide [(4.67±0.71) and (22.5±2.58) m~2/μm] significantly (P 0.01).No difference was observed in the improvement of airway remodeling and vascular remodeling between RG and BG.There were a significant negative correlation between nuclear PPARγ and collagen deposition around vessel (r =-0.91,P0.01),but not the thickness of vascular wall in the 4 groups except for BG.Conclusions Rosiglitazone,a PPARγ agonist,inhibited the airway vascular remodeling as budesonide in asthmatic mice.