NDLI: Toluhydroquinone from Aspergillus sp. suppress inflammatory mediators via nuclear factor-κB and mitogen-activated protein kinases pathways in lipopolysaccharide-induced RAW264.7 cells.

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Toluhydroquinone from Aspergillus sp. suppress inflammatory mediators via nuclear factor-κB and mitogen-activated protein kinases pathways in lipopolysaccharide-induced RAW264.7 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hwang, Dukhyun Son, Byeng-Wha Shin, Pyung-Gyun Choi, Jae-Sue Seo, Yong-Bae Kim, Gun-Do
Description	Country affiliation: South Korea Author Affiliation: Hwang D ( Department of Microbiology, College of Natural Sciences, Pukyong National University, Busan, South Korea.); Son BW ( Department of Chemistry, College of Natural Sciences, Pukyong National University, Busan, South Korea.); Shin PG ( Rural Development Administration, National Institute of Horticultural and Herbal Science, Suwon, South Korea.); Choi JS ( Department of Food and Nutrition, Pukyong National University, Busan, South Korea.); Seo YB ( Institute of Fisheries Science, College of Fisheries Science, Pukyong National University, Busan, South Korea.); Kim GD ( Department of Microbiology, College of Natural Sciences, Pukyong National University, Busan, South Korea.)
Abstract	OBJECTIVES: The purpose of this study is to investigate anti-inflammatory effects of toluhydroquinone in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. METHODS: Toluhydroquinone was purified from a fungal strain, Aspergillus sp. We investigated that levels of nitric oxide (NO) using Griess reagent, production of prostaglandin E2 (PGE2 ) and pro-inflammatory cytokines using ELISA assay. We conducted Western blot analysis to investigate regulatory effects of toluhydroquinone on expression of inducible nitric oxide synthase (iNOS), cyclooxyganse-2 (COX-2), nuclear factor-κB (NF-κB), Akt and mitogen-activated protein kinases (MAPKs) in LPS-stimulated RAW264.7 cells. The translocation of NF-κB was detected by immunofluorescence staining. KEY FINDINGS: Toluhydroquinone inhibited production of NO and PGE2 via suppressing protein expression of iNOS and COX-2, respectively. Secretion and expression of inflammatory cytokines were down-regulated by toluhydroquinone as well. Toluhydroquinone reduced phosphorylation of Akt, NF-κB and MAPKs. Moreover, toluhydroquinone inhibited translocation of NF-κB from the cytosol into the nucleus. CONCLUSIONS: We revealed that inhibitory effects of toluhydroquinone on expression of inflammatory mediators are induced through inactivation of Akt, NF-κB and MAPKs. Thus, our results suggest that toluhydroquinone may be used for a potential anti-inflammatory reagent.
File Format	HTM / HTML
ISSN	00223573
Issue Number	9
Volume Number	67
e-ISSN	20427158
Journal	Journal of Pharmacy and Pharmacology
Language	English
Publisher	Wiley
Publisher Date	2015-09-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Pharmacology Anti-inflammatory Agents Pharmacology Aspergillus Metabolism Benzoquinones Inflammation Drug Therapy Lipopolysaccharides Mitogen-activated Protein Kinases Nf-kappa B Animals Cell Line Cyclooxygenase 2 Dinoprostone Hek293 Cells Humans Chemically Induced Macrophages Drug Effects Mice Nitric Oxide Nitric Oxide Synthase Type Ii Phosphorylation Signal Transduction Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pharmacology Pharmaceutical Science

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