Magnolol ameliorates lipopolysaccharide-induced acute lung injury in rats through PPAR-γ-dependent inhibition of NF-kB activation

Acute lung injury (ALI) has a high morbidity and mortality rate due to the serious inflammation and edema occurred in lung. Magnolol extracted from Magnolia officinalis, has been reported to exhibit anti-inflammatory, and antioxidant activities. Peroxisome proliferator-activated receptors (PPARs) are known to exert a cytoprotective effect against cellular inflammatory stress and oxidative injury. The aim of this study was to explore the involvement of PPAR-gamma in the beneficial effect of magnolol in lipopolysaccharide (LPS)-induced ALI. We found that treatment with magnolol greatly improved the pathological features of ALI evidenced by reduction of lung edema, polymorphonuclear neutrophil infiltration, ROS production, the levels of pro-inflammatory cytoldnes in bronchoalveolar lavage fluid (BALF), the expression of iNOS and COX-2, and NF-kappa B activation in lungs exposed to LPS. Importantly, magnolol is capable of increasing the PPAR-gamma expression and activity in lungs of ALL However, blocking PPAR-gamma activity with GW9662 markedly abolished the protective and anti-inflammatory effects of magnolol. Taken together, the present study provides a novel mechanism accounting for the protective effect of magnolol in LPS-induced AU is at least partly attributed to induction of PPAR-gamma in lungs, and in turn suppressing NF-kappa B-related inflammatory responses. (C) 2015 Elsevier B.V. All rights reserved.