title: Inhibition of 5-lipoxygenase and cyclooxygenase-2 pathways by pain-relieving plaster in macrophages.
abstract: BACKGROUND
  Pain-relieving plaster (PRP) is a traditional Chinese medicine (TCM) that has been widely used with satisfactory results in the treatment of some diseases related to inflammation, such as bruises, chronic arthritis.
  
  
  OBJECTIVE
  The mechanisms underlying the anti-inflammatory actions of PRP are investigated in this study for the first time.
  
  
  METHODS
  The anti-inflammatory effects of PRP extracts were evaluated in lipopolysaccharide (LPS) or calcium ionophore A23187-treated murine peritoneal macrophages (PMs). Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), prostaglandin E₂ (PGE₂), and leukotrienes B₄ (LTB₄) were evaluated by ELISA assays. Reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot analysis were used to detect the expression of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX). Nuclear factor-kappa B (NF-κB)-DNA-binding activity was determined by gel mobility shift assay.
  
  
  RESULTS
  PRP extracts were found to inhibit the production of TNF-α, IL-1β, and PGE(2), reduce the expressions of COX-2 at the mRNA and protein levels induced by LPS, and reduced the production of LTB₄ induced by A23187. Furthermore, PRP extracts significantly attenuated LPS-induced NF-κB-DNA-binding activity.
  
  
  CONCLUSIONS
  The anti-inflammatory effects of PRP possibly are related to reduction of inflammatory cytokines (TNF-α and IL-1β), inducible inflammatory enzyme (COX-2), and its metabolite PGE₂ via NF-κB signal pathway. Moreover, PRP extracts also notably inhibited the production of LTB₄, indicating that PRP inhibited the 5-LOX pathway, which may be the other mechanism for its anti-inflammatory action.
authors.affiliation: Department of pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
authors.forename: Shan-Ying
authors.initials: SY
authors.lastname: Peng
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: Xu-hong
authors.initials: XH
authors.lastname: Bao
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Fu-ying
authors.initials: FY
authors.lastname: Zhang
authors.forename: Feng
authors.initials: F
authors.lastname: Wang
authors.forename: Wen-jie
authors.initials: WJ
authors.lastname: Wang
mesh_terms: D000279:Administration, Cutaneous; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000494:pharmacology*; D001094:Arachidonate 5-Lipoxygenase / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D004008:Diclofenac / Q000494:pharmacology; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000494:pharmacology*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008516:Medicine, Chinese Traditional; D051379:Mice; D008810:Mice, Inbred C57BL; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D004365:Drugs, Chinese Herbal; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D004008:Diclofenac; D001094:Arachidonate 5-Lipoxygenase; D051546:Cyclooxygenase 2