El-Naa M.M.El-Refaei M.F.Nasif W.A.Abduljawad S.H.El-Brairy A.I.El-Readi M.Z.Department of Pharmacology and ToxicologyFaculty of PharmacyOctober University for Modern Sciences and Arts6 October CityEgypt; Molecular Biology DepartmentInstitute of Genetic Engineering and BiotechnologySadat City UniversitySadat CityEgypt; Department of BiochemistryFaculty of PharmacyAl-Azhar UniversityAssiutEgypt; Department of BiochemistryFaculty of MedicineUmm Al-Qura UniversityMakkahSaudi Arabia; Department of Food SciencesFaculty of Family ScienceTaibah UniversityAl Madinah Al-MunawarahSaudi Arabia; Department of Clinical BiochemistryFaculty of MedicineUmm Al-Qura UniversityP.O. Box 13174AbdiaMakkah21955Saudi Arabia2020-01-092020-01-092015223573https://doi.org/10.1111/jphp.12445PubMed ID 26099551https://t.ly/GgZkmScopusObjectives Peroxisome proliferator activated receptor-gamma (PPAR-?) has been shown to play an important role in the control of immunological and inflammatory responses. This study aims at investigating the potential role of rosiglitazone, a strong PPAR-? agonist in a murine model of bronchial asthma. Methods Adult male Guinea pigs were administered ovalbumin 100 mg/kg subcutaneous (SC) and 100 mg/kg intraperitoneal (IP). Treatment with rosiglitazone [5 mg/kg/day, per oral (PO)] was assessed for 21 days. On day 21, the animals were challenged with the same dose of ovalbumin. The forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC), FEV1/FVC, was measured using a spirometer to diagnosis lung obstruction. Serum levels of interleukin-5 (IL-5) and immunoglobulin E (IgE) were assessed. The activity of superoxide dismutase (SOD) and catalase and the level of reduced glutathione (GSH) were determined in lung tissue homogenates. Key findings Our results demonstrated that treatment with rosiglitazone resulted in a statistically significant improvement in lung function and histopathological features. Significant decrease in the serum levels of IL-5 and IgE were observed. The activity of SOD and catalase as well as the GSH level were significantly increased in the lung tissues of treated animals compared with untreated asthmatic animals. Serum IgE concentrations and IL-5 levels were directly correlated to each other and inversely correlated to the SOD, GSH and catalase levels in the all studied Guinea pigs. Conclusions Our results provide evidence that the PPAR-? agonist rosiglitazone may have potential in the development of therapies for bronchial asthma. 2015 Royal Pharmaceutical Society.EnglishOctober University for Modern Sciences and ArtsUniversity for Modern Sciences and ArtsMSA Universityجامعة أكتوبر للعلوم الحديثة والآدابbronchial asthmaimmunoglobulin Einterleukin-5peroxisome proliferator-activated receptor-gammarosiglitazonecatalasecholesterolglucoseglutathionehigh density lipoprotein cholesterolimmunoglobulin Elow density lipoprotein cholesterolperoxisome proliferator activated receptor gammarosiglitazonesuperoxide dismutasetriacylglycerol2,4 thiazolidinedione derivativeantiinflammatory agentantioxidantcatalaseglutathioneimmunoglobulin Einterleukin 5ovalbuminperoxisome proliferator activated receptor gammarosiglitazonesuperoxide dismutaseadultanimal experimentanimal modelanimal tissueantiinflammatory activityantioxidant activityArticleasthmacholesterol blood levelcontrolled studydown regulationdrug determinationdrug structureenzyme activityforced expiratory volumeforced vital capacityglucose blood levelguinea pighistopathologyimmune responsein vivo studylung functionlung function testlung homogenatemalenonhumanoxidative stressprotein blood leveltreatment responsetriacylglycerol blood levelagonistsanimalblooddisease modelimmunologymetabolismpathophysiologyAnimalsAnti-Inflammatory AgentsAntioxidantsAsthmaCatalaseDisease Models, AnimalGlutathioneGuinea PigsImmunoglobulin EInterleukin-5MaleOvalbuminPPAR gammaSuperoxide DismutaseThiazolidinedionesIn-vivo antioxidant and anti-inflammatory activity of rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonists in animal model of bronchial asthma.Articlehttps://doi.org/10.1111/jphp.12445PubMed ID 26099551