Evaluation of the antifibrotic effect of fenofibrate and rosiglitazone on bleomycin-induced pulmonary fibrosis in rats

Pan-PPAR agonist IVA337 is effective in experimental lung fibrosis and pulmonary hypertension

“…The advantage to target several PPAR isoforms has been previously suggested by the study of concomitant administration of fenofibrate (PPARα agonist) and rosiglitazone (PPARγ agonist), which enhanced the beneficial effects produced by either fenofibrate or rosiglitazone alone on bleomycin-induced lung fibrosis 5. Concomitant administration of low doses of fenofibrate and rosiglitazone also provided synergistic renoprotective effect against the development of diabetes-induced nephropathy and fibrosis 23.…”

Anti-Fibrotic Potential of Nicorandil in the Treatment of Bleomycin Induced Pulmonary Fibrosis

“…In addition, several studies have demonstrated that bleomycin administration in rats decreased the anti-oxidative capacity and increased oxidative stress in the lung tissue, which aggravated pulmonary fibrosis. 13,14,15 It has been established that in bleomycin induced pulmonary fibrosis the levels of the biochemical, oxidant and antioxidant parameters changed significantly than those of the normal levels. This is evident by increased levels Lactate Dehydrogenase (LDH) which is a marker of biochemical index.…”

“…Previous studies demonstrated that anti-oxidant agents ameliorated the accumulation of leukocytes in bronchial lavage fluid and lung tissue which agrees with our findings. [12][13][14][15][16][17][18][19] The pathophysiology of Bleomycin-induced lung injury typically consisted of two overlapping stages; an early inflammatory phase characterized by leukocyte infiltration and injury to alveolar epithelial cells, and a subsequent fibro-proliferative phase with matrix remodeling and fibrosis. 20 Haematoxylin & Eosin (H&E) staining results in BLM control group showed that acute inflammations were prominent with moderate or severe hemorrhage, widened alveolar septa, and infiltration of numerous inflammatory cells predominated by macrophages, neutral granulocytes, and lymphocytes.…”

The Myofibroblast: TGFβ-1, A Conductor which Plays a Key Role in Fibrosis by Regulating the Balance between PPARγ and the Canonical WNT Pathway

“…Overexpression of PPARγ suppresses the inhibition of its own transcriptional activity induced by TGF-β1 [162]. TZDs can inhibit lung fibrosis induced by bleomycin [97,169,174,185].…”