title: Inhibitory effects of salidroside on nitric oxide and prostaglandin E₂ production in lipopolysaccharide-stimulated RAW 264.7 macrophages.
abstract: The aim of this study was to evaluate the effect of salidroside on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E₂ (PGE₂) production in RAW 264.7 macrophages and related anti-inflammatory mechanism. PGE₂ production was measured by enzyme-linked immunosorbent assay (ELISA); NO production was tested by Griess reagent. Inducible nitric oxidesynthase (iNOS) and COX-2 were determined by RT-PCR and Western blot analysis; IκB and P-IκB protein express were detected by Western blot analysis; cytosolic free Ca²⁺ ([Ca²⁺](i)) was measured by a fluorescent microscope. The data showed salidroside inhibited LPS-induced NO and PGE₂ production and reduced iNOS and COX-2 protein expression in RAW 264.7 macrophages. Consistent with these observations, salidroside inhibited LPS-induced cytosolic free Ca²⁺ concentration ([Ca²⁺](i)) elevation. In addition, we further investigated signal transduction mechanisms and found that the activation of NF-κB was suppressed by salidroside in a dose-dependent manner. These results suggest that salidroside suppresses NO and PGE₂ production by inhibiting iNOS and COX-2 protein expression, level of [Ca²⁺](i), and activation of NF-κB signal transduction pathway.
authors.affiliation: 1 Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University , Changchun, Jilin, China .
authors.forename: Bocui
authors.initials: B
authors.lastname: Song
authors.forename: Guoren
authors.initials: G
authors.lastname: Huang
authors.forename: Ying
authors.initials: Y
authors.lastname: Xiong
authors.forename: Jingbo
authors.initials: J
authors.lastname: Liu
authors.forename: Linli
authors.initials: L
authors.lastname: Xu
authors.forename: Zhenning
authors.initials: Z
authors.lastname: Wang
authors.forename: Gen
authors.initials: G
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Lu
authors.forename: Shuang
authors.initials: S
authors.lastname: Guan
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D015232:Dinoprostone / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010636:Phenols / Q000494:pharmacology* / Q000627:therapeutic use; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D029771:Rhodiola / Q000737:chemistry*; D015398:Signal Transduction
chemical_list: D000893:Anti-Inflammatory Agents; D052246:Cyclooxygenase 2 Inhibitors; D005960:Glucosides; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010636:Phenols; D010936:Plant Extracts; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D015232:Dinoprostone; C009172:rhodioloside; D002118:Calcium