کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5832277 | 1122593 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Activation of Nrf2/HO-1signaling pathway involves the anti-inflammatory activity of magnolol in Porphyromonas gingivalis lipopolysaccharide-stimulated mouse RAW 264.7 macrophages
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کلمات کلیدی
NF-κBNRF-2P. gingivalisHeme oxygenase-1IKKDAPIiNOSRANKLCOX-2HO-1NACLPSFITC4′,6′-diamidino-2-phenylindole - 4 '، 6'-diamidino-2-phenylindolekeap1 - buy1IκB kinase - IkB kinaseMAPKs - MAPK هاN-acetyl-cysteine - N-استیل سیستئینROS - ROSSnPP - SNPPinflammation - التهاب( توروم) inducible nitric oxide synthase - سنتاز اکسید نیتریک القاییCyclooxygenase-2 - سیکلوکوکسیژناز2Nuclear factor-erythroid 2-related factor 2 - عامل فاکتور هسته ای - عامل 2 وابسته به erythroid 2antioxidant response element - عنصر پاسخ آنتی اکسیدانNuclear factor-kappa B - فاکتور هسته ای-کاپا Bfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتlipopolysaccharide - لیپوپلی ساکاریدMagnolol - مگنولولARE - هستندKelch-like ECH-associated protein 1 - پروتئین مرتبط با ECH کلچ 1tin protoporphyrin IX - پروتوپورفیرین IXPorphyromonas gingivalis - ژنژیوالیس پورفیروموناسmitogen-activated protein kinases - کیناز پروتئین فعال MitogenReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
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 Porphyromonas 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 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 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 29, Issue 2, December 2015, Pages 770-778
Journal: International Immunopharmacology - Volume 29, Issue 2, December 2015, Pages 770-778
نویسندگان
Sheng-Hua Lu, Wen-Lin Hsu, Tso-Hsiao Chen, Tz-Chong Chou,