PMID- 21639685
OWN - NLM
STAT- MEDLINE
DCOM- 20110929
LR  - 20220408
IS  - 1744-5116 (Electronic)
IS  - 1388-0209 (Linking)
VI  - 49
IP  - 7
DP  - 2011 Jul
TI  - Inhibition of 5-lipoxygenase and cyclooxygenase-2 pathways by pain-relieving 
      plaster in macrophages.
PG  - 716-26
LID - 10.3109/13880209.2010.544043 [doi]
AB  - 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-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E(2) (PGE(2)), and 
      leukotrienes B(4) (LTB(4)) 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-kappaB)-DNA-binding activity was determined by 
      gel mobility shift assay. RESULTS: PRP extracts were found to inhibit the 
      production of TNF-alpha, IL-1beta, and PGE(2), reduce the expressions of COX-2 at the 
      mRNA and protein levels induced by LPS, and reduced the production of LTB(4) 
      induced by A23187. Furthermore, PRP extracts significantly attenuated LPS-induced 
      NF-kappaB-DNA-binding activity. DISCUSSION AND CONCLUSION: The anti-inflammatory 
      effects of PRP possibly are related to reduction of inflammatory cytokines (TNF-alpha 
      and IL-1beta), inducible inflammatory enzyme (COX-2), and its metabolite PGE(2) via 
      NF-kappaB signal pathway. Moreover, PRP extracts also notably inhibited the 
      production of LTB(4), indicating that PRP inhibited the 5-LOX pathway, which may be 
      the other mechanism for its anti-inflammatory action.
FAU - Peng, Shan-Ying
AU  - Peng SY
AD  - Department of pharmacology, Institute of Materia Medica, Chinese Academy of 
      Medical Sciences & Peking Union Medical College, Beijing, China.
FAU - Liu, Yang
AU  - Liu Y
FAU - Bao, Xu-hong
AU  - Bao XH
FAU - Wang, Lin
AU  - Wang L
FAU - Zhang, Fu-ying
AU  - Zhang FY
FAU - Wang, Feng
AU  - Wang F
FAU - Wang, Wen-jie
AU  - Wang WJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Pharm Biol
JT  - Pharmaceutical biology
JID - 9812552
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 144O8QL0L1 (Diclofenac)
RN  - EC 1.13.11.34 (Arachidonate 5-Lipoxygenase)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Administration, Cutaneous
MH  - Animals
MH  - Anti-Inflammatory Agents/administration & dosage/*pharmacology
MH  - Arachidonate 5-Lipoxygenase/*drug effects/genetics/metabolism
MH  - Cyclooxygenase 2/*drug effects/genetics/metabolism
MH  - Diclofenac/pharmacology
MH  - Drugs, Chinese Herbal/administration & dosage/*pharmacology
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Inflammation/drug therapy/physiopathology
MH  - Interleukin-1beta/antagonists & inhibitors/metabolism
MH  - Macrophages, Peritoneal/drug effects/metabolism
MH  - Male
MH  - Medicine, Chinese Traditional
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/metabolism
EDAT- 2011/06/07 06:00
MHDA- 2011/10/01 06:00
CRDT- 2011/06/07 06:00
PHST- 2011/06/07 06:00 [entrez]
PHST- 2011/06/07 06:00 [pubmed]
PHST- 2011/10/01 06:00 [medline]
AID - 10.3109/13880209.2010.544043 [doi]
PST - ppublish
SO  - Pharm Biol. 2011 Jul;49(7):716-26. doi: 10.3109/13880209.2010.544043.