A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia.

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Abstract Text:

Mohamed G Bani-Hani,David Greenstein,Brian E Mann,Colin J Green,Roberto Motterlini,Mohamed G Bani-Hani,David Greenstein,Brian E Mann,Colin J Green,Roberto Motterlini,

The development of carbon monoxide-releasing molecules (CO-RMs) in recent years helped to shed more light on the diverse range of anti-inflammatory and cytoprotective activities of CO gas. In this study, we examined the effect of a ruthenium-based water-soluble CO carrier (CORM-3) on lipopolysaccharide (LPS)- and interferon-gamma (INF-gamma)-induced inflammatory responses in BV-2 microglial cells and explored the possible mechanisms of action. BV-2 microglial cells were stimulated with either LPS or INF-gamma in the presence of CORM-3 and the inflammatory response evaluated by assessing the effect on nitric oxide production (nitrite levels) and tumor necrosis factor-alpha (TNF-alpha) release. Similar experiments were also performed in the presence of inhibitors of guanylate cyclase (ODQ), NO synthase (L-NAME), heme oxygenase activity (tin protoporphyrin IX) or various mitogen-activated protein kinase (MAPK) inhibitors. CORM-3 significantly attenuated the inflammatory response to LPS and INF-gamma as evidenced by a significant reduction (p < 0.001) in nitrite levels and TNF-alpha production (P < 0.05). Such effect was maintained in the presence of ODQ, L-NAME or tin protoporphyrin without showing any cytotoxicity. The use of an inactive form of CORM-3 that does not contain carbonyl groups (Ru(DMSO)(4)Cl(2) failed to inhibit the increase in inflammatory markers suggesting that liberated CO mediates the observed effects. In addition, inhibition of phosphatidylinositol-3-phosphate kinase (PI3K) and extracellular signal-regulated kinase (ERK) pathways seemed to amplify the anti-inflammatory effect of CORM-3, particularly in cells stimulated with INF-gamma. These results suggest that the anti-inflammatory action of CORM-3 could be exploited to mitigate microglia activation in neuro-inflammatory diseases.

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Publishing Authors By Initials

MG Bani-Hani,D Greenstein,BE Mann,CJ Green,R Motterlini,MG Bani-Hani,D Greenstein,BE Mann,CJ Green,R Motterlini,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Pharmacological reports : PR

VOLUME: 58 Suppl

Page Numbers: 132-44

Journal Abbreviation:

ISSN: 1734-1140

DAY: 2

MONTH: 03

YEAR: 2006

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101234999

A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia.

AFFILIATION: Vascular Biology Unit, Department of Surgical Research, Northwick Park Institute for Medical Research, Harrow, United Kingdom.

Country: Poland

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Pharmacol Rep

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

A carbon monoxide-releasing molecule CORM-3 attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia Related Publications

• A carbon monoxide-releasing molecule (CORM-3) attenuates lipopolysaccharide- and interferon-gamma-induced inflammation in microglia.
• A cytoprotective role for the heme oxygenase-1/CO pathway during neural differentiation of human mesenchymal stem cells.
• CO and NO in medicine.
• Carbon monoxide-releasing molecules (CO-RMs): vasodilatory, anti-ischaemic and anti-inflammatory activities.
• Carbon monoxide-releasing molecules: a pharmacological expedient to counteract inflammation.
• Eta(1)-2-pyrone metal carbonyl complexes as CO-releasing molecules (CO-RMs): a delicate balance between stability and CO liberation.
• Improved myocardial function after cold storage with preservation solution supplemented with a carbon monoxide-releasing molecule (CORM-3).
• Mitochondrial and cellular heme-dependent proteins as targets for the bioactive function of the heme oxygenase/carbon monoxide system.
• Structure-activity relationships of methoxychalcones as inducers of heme oxygenase-1.
• Use of carbon monoxide as a therapeutic agent: promises and challenges.
• [(Eta-C5H4R)Fe(CO)2X], X = Cl, Br, I, NO3, CO2Me and [(eta-C5H4R)Fe(CO)3]+, R = (CH2)nCO2Me (n = 0-2), and CO2CH2CH2OH: a new group of CO-releasing molecules.