Paper Title
Inhibitory Effects of Magnolol on Inflammatory Mediator Production by Porphyromonasgingivalis Lipopolysaccharide in Mouse Raw 264.7 Macrophages Via Nrf-2 Mediated Heme Oxygenase-1 Signaling Pathways

Abstract
Magnolol isolated from Magnolia officinalis, a Chinese medical herb, exhibits an anti-inflammatory activity and a protective effect against periodontitis. The inflammation caused by lipopolysaccharide (LPS) from Porphyromonasgingivalis (P. gingivalis) has been considered a key inducer in the development of priodontitis. In this study, we investigated whether magnolol inhibits P. gingivalis LPS-evoked inflammatory responses in RAW 264.7 macrophages and the involvement of heme oxygenase-1 (HO-1). In P. gingivalis LPS-stimulated macrophages, magnolol treatment remarkably inhibited the inflammatory responses evidenced by suppression of pro-inflammatory cytokine, prostaglandin E2, nitrite formation, and the expression of inducible nitric oxide synthase and cyclooxygenase-2, as well as NF-κB activation accompanied by a significant elevation of Nrf-2 nuclear translocation and HO-1 expression/activity. However, inhibiting HO-1 activity with tin protoporphyrin IX (SnPP) markedly reversed the anti-inflammatory effects of magnolol. Collectively, these findings provide a novel mechanism by which magnolol inhibits P. gingivalis LPS-induced inflammation in macrophages is at least partly mediated by HO-1 activation, and thereby promoting its clinical use in periodontitis. Keywords� Magnolol, Porphyromonasgingivalis, Lipopolysaccharide, Heme Oxygenase-1, Inflammation.