Biliverdin and bilirubin sulfonate inhibit monosodium urate induced sterile inflammation in the rat.

Bile pigments Bilirubin sulfonate Biliverdin Cytokines Gout Monosodium urate Sterile inflammation

Journal

European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
ISSN: 1879-0720
Titre abrégé: Eur J Pharm Sci
Pays: Netherlands
ID NLM: 9317982

Informations de publication

Date de publication:
01 Dec 2020
Historique:
received: 09 02 2020
revised: 07 08 2020
accepted: 31 08 2020
pubmed: 15 9 2020
medline: 22 6 2021
entrez: 14 9 2020
Statut: ppublish

Résumé

Biliverdin, a by-product of haem catabolism, possesses potent endogenous antioxidant and anti-inflammatory properties. Bilirubin-C10-sulfonate (BRS), an active metabolite formed after enteral administration of BV in the rat, also possess antioxidant properties. Therefore, we investigated the anti-inflammatory and antioxidant activity of BV and BRS in an in vivo model of monosodium urate induced sterile inflammation. Subcutaneous air pouches were created on the dorsal flanks of Wistar rats (10-12 weeks of age). Prior to stimulation of the 6-day old pouch with monosodium urate (25 mg), groups were pre-treated with intraperitoneal BRS (27 mg/kg) and BV (27 mg/kg). Total and differential leukocyte counts were determined in pouch fluid aspirate at 1, 6, 12, 24 and 48 h after monosodium urate stimulation. Biliverdin (BV), BRS and unconjugated bilirubin (UCB) concentrations in the serum and pouch fluid were quantified using liquid chromatography-mass spectrometry. Pouch fluid cytokine concentrations (IL-1β, IL-1α, TNF-α, IL-17A, IL-12, GM-CSF, IL-33, IFN-γ, IL-18, IL-10, MCP-1, CXCL-1 and IL-6) were assessed after 6 h. In addition, 24 h protein carbonyl and chloramine concentrations were assessed in pouch fluid using ELISA and spectrophotometry, respectively. BRS and BV significantly (p < 0.05) inhibited leukocyte (total, neutrophil and macrophage) infiltration into the pouch fluid from 6 to 48 h. For example, after 6 h neutrophil counts decreased following BRS (0.32 ± 0.11 × 10 This study is the first to elucidate anti-inflammatory activity of BRS and the efficacy of BV administration in a model of gouty inflammation. Reduced leukocyte infiltration and cytokine production in response to sterile inflammation further support the importance of these molecules in physiology and their therapeutic potential in sterile inflammation.

Sections du résumé

BACKGROUND BACKGROUND
Biliverdin, a by-product of haem catabolism, possesses potent endogenous antioxidant and anti-inflammatory properties. Bilirubin-C10-sulfonate (BRS), an active metabolite formed after enteral administration of BV in the rat, also possess antioxidant properties. Therefore, we investigated the anti-inflammatory and antioxidant activity of BV and BRS in an in vivo model of monosodium urate induced sterile inflammation.
METHODS METHODS
Subcutaneous air pouches were created on the dorsal flanks of Wistar rats (10-12 weeks of age). Prior to stimulation of the 6-day old pouch with monosodium urate (25 mg), groups were pre-treated with intraperitoneal BRS (27 mg/kg) and BV (27 mg/kg). Total and differential leukocyte counts were determined in pouch fluid aspirate at 1, 6, 12, 24 and 48 h after monosodium urate stimulation. Biliverdin (BV), BRS and unconjugated bilirubin (UCB) concentrations in the serum and pouch fluid were quantified using liquid chromatography-mass spectrometry. Pouch fluid cytokine concentrations (IL-1β, IL-1α, TNF-α, IL-17A, IL-12, GM-CSF, IL-33, IFN-γ, IL-18, IL-10, MCP-1, CXCL-1 and IL-6) were assessed after 6 h. In addition, 24 h protein carbonyl and chloramine concentrations were assessed in pouch fluid using ELISA and spectrophotometry, respectively.
RESULTS RESULTS
BRS and BV significantly (p < 0.05) inhibited leukocyte (total, neutrophil and macrophage) infiltration into the pouch fluid from 6 to 48 h. For example, after 6 h neutrophil counts decreased following BRS (0.32 ± 0.11 × 10
CONCLUSIONS CONCLUSIONS
This study is the first to elucidate anti-inflammatory activity of BRS and the efficacy of BV administration in a model of gouty inflammation. Reduced leukocyte infiltration and cytokine production in response to sterile inflammation further support the importance of these molecules in physiology and their therapeutic potential in sterile inflammation.

Identifiants

pubmed: 32927072
pii: S0928-0987(20)30334-1
doi: 10.1016/j.ejps.2020.105546
pii:
doi:

Substances chimiques

Uric Acid 268B43MJ25
Biliverdine O9MIA842K9
Bilirubin RFM9X3LJ49

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

105546

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Ryan G Shiels (RG)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

Wenu Hewage (W)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

Evan N Pennell (EN)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

Josif Vidimce (J)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

Gary Grant (G)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia.

Andrew G Pearson (AG)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

Karl-Heinz Wagner (KH)

Department of Nutritional Sciences, University of Vienna, Vienna, Austria.

Michael Morgan (M)

Department of Anatomy and Neuroscience, University of Melbourne, Melbourne, Victoria, Australia.

Andrew C Bulmer (AC)

School of Medical Science, Griffith University, Gold Coast, Queensland, Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia. Electronic address: a.bulmer@griffith.edu.au.

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Classifications MeSH