Skip to main content Skip to search
Inhibition of 5-lipoxygenase and cyclooxygenase-2 pathways by pain-relieving plaster in macrophages
Pharmaceutical Biology
Format: Journal Article
Publication Date: Nov 30, 2010
Pages: 716 - 726
Sources ID: 105971
Visibility: Public (group default)
Abstract: (Show)
Context: 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. Materials and 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-αÎł (TNF-αÎł), interleukin-1βÎø (IL-1βÎø), 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-κÎðB)--DNA-binding activity was determined by gel mobility shift assay. Results: PRP extracts were found to inhibit the production of TNF-αÎł, IL-1βÎø, and PGE2, 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-κÎðB--DNA-binding activity. Discussion and conclusion: The anti-inflammatory effects of PRP possibly are related to reduction of inflammatory cytokines (TNF-αÎł and IL-1βÎø), inducible inflammatory enzyme (COX-2), and its metabolite PGE2 via NF-κÎðB 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.