Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 29, Issue 2, Pages 770-778Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.08.042
Keywords
Magnolol; Porphyromonas gingivalis; Lipopolysaccharide; Heme oxygenase-1; Inflammation
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Funding
- National Science Council of Taiwan, Republic of China [NSC 97-2320-B-016-008-MY3]
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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 Poiphyromonas gingivalis (P. gingivalis) has been considered a key inducer in the development of periodontitis. 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). Magnolol significantly activated p38 MAPK, Nrf-2/HO-1 cascade and reactive oxygen species (ROS) formation. Notably, the Nrf-2 activation and HO-1 induction by magnolol were greatly diminished by blocking p38 MAPK activity and ROS production. Furthermore, in P. gingivalis LPS-stimulated macrophages, magnolol treatment remarkably inhibited the inflammatory responses evidenced by suppression of pro-inflammatory cytoldne, prostaglandin E-2, nitrite formation, and the expression of inducible nitric oxide synthase and cyclooxygenase-2, as well as NF-kappa B 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 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. (C) 2015 Elsevier B.V. All rights reserved.
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