Anti-inflammatory effects of Phytodolor® (STW 1) and components (poplar, ash and goldenrod) on human monocytes/macrophages.


Journal

Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794

Informations de publication

Date de publication:
May 2019
Historique:
received: 11 06 2018
revised: 30 01 2019
accepted: 17 02 2019
pubmed: 5 3 2019
medline: 28 7 2019
entrez: 5 3 2019
Statut: ppublish

Résumé

Populus tremula L. (Poplar), Fraxinus excelsior L. (ash) and Solidago virgaurea L. (goldenrod) have been used for medicinal purposes through centuries, to treat pain, fever and inflammation, but their mechanisms of action are still not fully understood. The present study was performed to investigate, whether the herbal medicinal product Phytodolor Adherent human monocytes obtained from peripheral blood mononuclear cells (PBMCs) were cultured in serum-free medium and pre-treated with 50-100 µg/ml of diclofenac, STW 1, their components, poplar, ash or goldenrod or its combination (0.05% to 2%). Thereafter, monocytes were activated with 0.1 or 1 µg/ml LPS for 24 h. The intracellular expressions of TNF-α or PTGS2 were determined by cell-based ELISA. Apoptotic cells were identified by YO-PRO-1 staining. Protein or total RNA were isolated to perform SDS-PAGE/Western blot and qRT-PCR analyses. PMA-differentiated human THP-1 macrophages were pre-treated with diclofenac (50 µg/ml) or STW1 (0.1%) and afterwards with LPS (1 µg/ml) and the translocation of the intracellular p62 NF-κB subunit was detected by immunofluorescence. STW 1 inhibited the intracellular content of TNF-α and PTGS2 protein, as well as of TNF-α and PTGS2 gene expression and induced apoptosis in LPS-activated human monocytes under serum free conditions. Furthermore, STW 1 inhibited the translocation of the p65 subunit of the redox-regulated NF-κB into the nucleus in LPS-activated human macrophages. The present in vitro investigations suggest a significant anti-inflammatory activity of STW 1 and its components by inhibiting pro-inflammatory cytokine as TNF-α and the key enzyme PTGS2 in LPS-activated human monocytes, which is, at least partly mediated through the suppression of NF-κB activation. Our results provide evidence for distinctive anti-inflammatory effects of STW 1 and its components on LPS-activated human monocytes/macrophages and, thus, for the therapeutic use of STW 1 in inflammation and pain related disorders.

Sections du résumé

BACKGROUND BACKGROUND
Populus tremula L. (Poplar), Fraxinus excelsior L. (ash) and Solidago virgaurea L. (goldenrod) have been used for medicinal purposes through centuries, to treat pain, fever and inflammation, but their mechanisms of action are still not fully understood. The present study was performed to investigate, whether the herbal medicinal product Phytodolor
METHODS METHODS
Adherent human monocytes obtained from peripheral blood mononuclear cells (PBMCs) were cultured in serum-free medium and pre-treated with 50-100 µg/ml of diclofenac, STW 1, their components, poplar, ash or goldenrod or its combination (0.05% to 2%). Thereafter, monocytes were activated with 0.1 or 1 µg/ml LPS for 24 h. The intracellular expressions of TNF-α or PTGS2 were determined by cell-based ELISA. Apoptotic cells were identified by YO-PRO-1 staining. Protein or total RNA were isolated to perform SDS-PAGE/Western blot and qRT-PCR analyses. PMA-differentiated human THP-1 macrophages were pre-treated with diclofenac (50 µg/ml) or STW1 (0.1%) and afterwards with LPS (1 µg/ml) and the translocation of the intracellular p62 NF-κB subunit was detected by immunofluorescence.
RESULTS RESULTS
STW 1 inhibited the intracellular content of TNF-α and PTGS2 protein, as well as of TNF-α and PTGS2 gene expression and induced apoptosis in LPS-activated human monocytes under serum free conditions. Furthermore, STW 1 inhibited the translocation of the p65 subunit of the redox-regulated NF-κB into the nucleus in LPS-activated human macrophages.
CONCLUSION CONCLUSIONS
The present in vitro investigations suggest a significant anti-inflammatory activity of STW 1 and its components by inhibiting pro-inflammatory cytokine as TNF-α and the key enzyme PTGS2 in LPS-activated human monocytes, which is, at least partly mediated through the suppression of NF-κB activation. Our results provide evidence for distinctive anti-inflammatory effects of STW 1 and its components on LPS-activated human monocytes/macrophages and, thus, for the therapeutic use of STW 1 in inflammation and pain related disorders.

Identifiants

pubmed: 30831466
pii: S0944-7113(19)30039-X
doi: 10.1016/j.phymed.2019.152868
pii:
doi:

Substances chimiques

Anti-Inflammatory Agents, Non-Steroidal 0
Lipopolysaccharides 0
NF-kappa B 0
Plant Extracts 0
TNF protein, human 0
Tumor Necrosis Factor-alpha 0
Phytodolor N 141444-11-3
Diclofenac 144O8QL0L1
Cyclooxygenase 2 EC 1.14.99.1
PTGS2 protein, human EC 1.14.99.1

Types de publication

Journal Article

Langues

eng

Pagination

152868

Informations de copyright

Copyright © 2019 The Author(s). Published by Elsevier GmbH.. All rights reserved.

Auteurs

Gabriel A Bonaterra (GA)

Anatomy und Cell Biology, Department of Medical Cell Biology, Philipps-University of Marburg, Robert-Koch-Str. 8, 35032 Marburg, Germany. Electronic address: gabriel.bonaterra@staff.uni-marburg.de.

Hans Schwarzbach (H)

Anatomy und Cell Biology, Department of Medical Cell Biology, Philipps-University of Marburg, Robert-Koch-Str. 8, 35032 Marburg, Germany.

Olaf Kelber (O)

Innovation and Development, Phytomedicine Supply and Development Centre, Bayer Consumer Health Care, Steigerwald Arzneimittel GmbH, Havelstraße 5, 64295 Darmstadt, Germany.

Dieter Weiser (D)

Innovation and Development, Phytomedicine Supply and Development Centre, Bayer Consumer Health Care, Steigerwald Arzneimittel GmbH, Havelstraße 5, 64295 Darmstadt, Germany.

Ralf Kinscherf (R)

Anatomy und Cell Biology, Department of Medical Cell Biology, Philipps-University of Marburg, Robert-Koch-Str. 8, 35032 Marburg, Germany.

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Classifications MeSH