Anti-inflammatory effects of the willow bark extract STW 33-I (Proaktiv(®)) in LPS-activated human monocytes and differentiated macrophages.
Identifieur interne : 001669 ( Main/Corpus ); précédent : 001668; suivant : 001670Anti-inflammatory effects of the willow bark extract STW 33-I (Proaktiv(®)) in LPS-activated human monocytes and differentiated macrophages.
Auteurs : G A Bonaterra ; E U Heinrich ; O. Kelber ; D. Weiser ; J. Metz ; R. KinscherfSource :
- Phytomedicine : international journal of phytotherapy and phytopharmacology [ 1618-095X ] ; 2010.
English descriptors
- KwdEn :
- Anti-Inflammatory Agents (pharmacology), Anti-Inflammatory Agents, Non-Steroidal (MeSH), Apoptosis (drug effects), Benzyl Alcohols (pharmacology), Biological Transport (drug effects), Cyclooxygenase 2 (genetics), Cyclooxygenase 2 (metabolism), Dose-Response Relationship, Drug (MeSH), Flavonoids (pharmacology), Glucosides (pharmacology), Lipopolysaccharides (MeSH), Macrophages (drug effects), Monocytes (drug effects), NF-kappa B (metabolism), Nitric Oxide (metabolism), Phenols (pharmacology), Plant Bark (MeSH), Plant Extracts (pharmacology), Polyphenols (MeSH), RNA, Messenger (metabolism), Salix (chemistry), Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , genetics : Cyclooxygenase 2, Tumor Necrosis Factor-alpha.
- chemical , metabolism : Cyclooxygenase 2, NF-kappa B, Nitric Oxide, RNA, Messenger, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Anti-Inflammatory Agents, Benzyl Alcohols, Flavonoids, Glucosides, Phenols, Plant Extracts.
- chemical : Anti-Inflammatory Agents, Non-Steroidal, Lipopolysaccharides, Polyphenols.
- chemistry : Salix.
- drug effects : Apoptosis, Biological Transport, Macrophages, Monocytes.
- Dose-Response Relationship, Drug, Plant Bark.
Abstract
INTRODUCTION
Willow bark extract is frequently used in the treatment of painful rheumatological diseases, such as arthritis and back pain. Its effect has been attributed to its main component salicin, but pharmacological studies have shown that the clinical efficacy of the willow bark extract cannot be explained by its salicin content alone. Therefore different modes of action have been suggested for the anti-inflammatory effect of willow bark extract. Here, we report in vitro data revelling the effect and mode of action of the aqueous willow bark extract STW 33-I as well as a water-soluble fraction (fraction E [Fr E]) in comparison with well-known non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin (ASA) and diclofenac (Diclo) on pro-inflammatorily activated human monocytes and differentiated macrophages.
RESULTS
STW 33-I and the water-soluble Fr E showed concentration-dependent and significant anti-inflammatory effects in lipopolysaccharide-activated monocytes. Both inhibited the intracellular protein expression of tumour necrosis factor-alpha (TNFα) as well as the mRNA expression of TNFα and cyclooxygenase 2 (COX-2), and the release of nitric oxide (NO). In addition, apoptosis of pro-inflammatorily activated monocytes was induced. Furthermore, treatment of activated macrophages with STW 33-I inhibited the nuclear translocation of the p65 subunit of the nuclear transcription factor-kappa B (NF-κB p65).
CONCLUSIONS
The present in vitro investigations suggest a significant anti-inflammatory activity of willow bark water extract STW 33-1 and of its water-soluble fraction by inhibiting pro-inflammatory cytokines (TNFα), COX-2 and nuclear translocation of the transcription factor NF-κB in pro-inflammatorily activated monocytes. Our results provide further evidence for the therapeutic use of STW 33-I in inflammation-related disorders.
DOI: 10.1016/j.phymed.2010.03.022
PubMed: 20570123
Links to Exploration step
pubmed:20570123Le document en format XML
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<affiliation><nlm:affiliation>Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Robert-Koch-Str. 8, 35032 Marburg, Germany. Gabriel.Bonaterra@medma.uni-heidelberg.de</nlm:affiliation>
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<author><name sortKey="Heinrich, E U" sort="Heinrich, E U" uniqKey="Heinrich E" first="E U" last="Heinrich">E U Heinrich</name>
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<author><name sortKey="Kelber, O" sort="Kelber, O" uniqKey="Kelber O" first="O" last="Kelber">O. Kelber</name>
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<author><name sortKey="Weiser, D" sort="Weiser, D" uniqKey="Weiser D" first="D" last="Weiser">D. Weiser</name>
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<author><name sortKey="Metz, J" sort="Metz, J" uniqKey="Metz J" first="J" last="Metz">J. Metz</name>
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<term>Anti-Inflammatory Agents, Non-Steroidal (MeSH)</term>
<term>Apoptosis (drug effects)</term>
<term>Benzyl Alcohols (pharmacology)</term>
<term>Biological Transport (drug effects)</term>
<term>Cyclooxygenase 2 (genetics)</term>
<term>Cyclooxygenase 2 (metabolism)</term>
<term>Dose-Response Relationship, Drug (MeSH)</term>
<term>Flavonoids (pharmacology)</term>
<term>Glucosides (pharmacology)</term>
<term>Lipopolysaccharides (MeSH)</term>
<term>Macrophages (drug effects)</term>
<term>Monocytes (drug effects)</term>
<term>NF-kappa B (metabolism)</term>
<term>Nitric Oxide (metabolism)</term>
<term>Phenols (pharmacology)</term>
<term>Plant Bark (MeSH)</term>
<term>Plant Extracts (pharmacology)</term>
<term>Polyphenols (MeSH)</term>
<term>RNA, Messenger (metabolism)</term>
<term>Salix (chemistry)</term>
<term>Tumor Necrosis Factor-alpha (genetics)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cyclooxygenase 2</term>
<term>Tumor Necrosis Factor-alpha</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclooxygenase 2</term>
<term>NF-kappa B</term>
<term>Nitric Oxide</term>
<term>RNA, Messenger</term>
<term>Tumor Necrosis Factor-alpha</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Benzyl Alcohols</term>
<term>Flavonoids</term>
<term>Glucosides</term>
<term>Phenols</term>
<term>Plant Extracts</term>
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<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term>
<term>Lipopolysaccharides</term>
<term>Polyphenols</term>
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<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Salix</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Biological Transport</term>
<term>Macrophages</term>
<term>Monocytes</term>
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<front><div type="abstract" xml:lang="en"><p><b>INTRODUCTION</b>
</p>
<p>Willow bark extract is frequently used in the treatment of painful rheumatological diseases, such as arthritis and back pain. Its effect has been attributed to its main component salicin, but pharmacological studies have shown that the clinical efficacy of the willow bark extract cannot be explained by its salicin content alone. Therefore different modes of action have been suggested for the anti-inflammatory effect of willow bark extract. Here, we report in vitro data revelling the effect and mode of action of the aqueous willow bark extract STW 33-I as well as a water-soluble fraction (fraction E [Fr E]) in comparison with well-known non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin (ASA) and diclofenac (Diclo) on pro-inflammatorily activated human monocytes and differentiated macrophages.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>STW 33-I and the water-soluble Fr E showed concentration-dependent and significant anti-inflammatory effects in lipopolysaccharide-activated monocytes. Both inhibited the intracellular protein expression of tumour necrosis factor-alpha (TNFα) as well as the mRNA expression of TNFα and cyclooxygenase 2 (COX-2), and the release of nitric oxide (NO). In addition, apoptosis of pro-inflammatorily activated monocytes was induced. Furthermore, treatment of activated macrophages with STW 33-I inhibited the nuclear translocation of the p65 subunit of the nuclear transcription factor-kappa B (NF-κB p65).</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>The present in vitro investigations suggest a significant anti-inflammatory activity of willow bark water extract STW 33-1 and of its water-soluble fraction by inhibiting pro-inflammatory cytokines (TNFα), COX-2 and nuclear translocation of the transcription factor NF-κB in pro-inflammatorily activated monocytes. Our results provide further evidence for the therapeutic use of STW 33-I in inflammation-related disorders.</p>
</div>
</front>
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<Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Willow bark extract is frequently used in the treatment of painful rheumatological diseases, such as arthritis and back pain. Its effect has been attributed to its main component salicin, but pharmacological studies have shown that the clinical efficacy of the willow bark extract cannot be explained by its salicin content alone. Therefore different modes of action have been suggested for the anti-inflammatory effect of willow bark extract. Here, we report in vitro data revelling the effect and mode of action of the aqueous willow bark extract STW 33-I as well as a water-soluble fraction (fraction E [Fr E]) in comparison with well-known non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin (ASA) and diclofenac (Diclo) on pro-inflammatorily activated human monocytes and differentiated macrophages.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">STW 33-I and the water-soluble Fr E showed concentration-dependent and significant anti-inflammatory effects in lipopolysaccharide-activated monocytes. Both inhibited the intracellular protein expression of tumour necrosis factor-alpha (TNFα) as well as the mRNA expression of TNFα and cyclooxygenase 2 (COX-2), and the release of nitric oxide (NO). In addition, apoptosis of pro-inflammatorily activated monocytes was induced. Furthermore, treatment of activated macrophages with STW 33-I inhibited the nuclear translocation of the p65 subunit of the nuclear transcription factor-kappa B (NF-κB p65).</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The present in vitro investigations suggest a significant anti-inflammatory activity of willow bark water extract STW 33-1 and of its water-soluble fraction by inhibiting pro-inflammatory cytokines (TNFα), COX-2 and nuclear translocation of the transcription factor NF-κB in pro-inflammatorily activated monocytes. Our results provide further evidence for the therapeutic use of STW 33-I in inflammation-related disorders.</AbstractText>
<CopyrightInformation>Copyright © 2010 Elsevier GmbH. All rights reserved.</CopyrightInformation>
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