Hydrogen sulfide‐releasing NSAIDs attenuate neuroinflammation induced by microglial and astrocytic activation
Identifieur interne : 001C17 ( Main/Exploration ); précédent : 001C16; suivant : 001C18Hydrogen sulfide‐releasing NSAIDs attenuate neuroinflammation induced by microglial and astrocytic activation
Auteurs : Moonhee Lee [Canada] ; Anna Sparatore [Italie] ; Piero Del Soldato [Italie] ; Edith Mcgeer [Canada] ; Patrick L. Mcgeer [Canada]Source :
- Glia [ 0894-1491 ] ; 2010-01-01.
English descriptors
- KwdEn :
- Air Pollutants (pharmacology), Analysis of Variance, Animals, Anti-Inflammatory Agents, Non-Steroidal (metabolism), Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Aspirin (pharmacology), Astrocytes (drug effects), Astrocytes (immunology), Astrocytes (metabolism), Cell Survival (drug effects), Cells, Cultured, Humans, Hydrogen Sulfide (metabolism), Interleukin-6 (metabolism), Intracellular Fluid (drug effects), Intracellular Fluid (metabolism), Lipopolysaccharides (pharmacology), Microglia (drug effects), Microglia (immunology), Microglia (metabolism), Neuroprotective Agents (pharmacology), Nitrites (metabolism), THP‐1 cells, Temporal Lobe (cytology), Time Factors, Tumor Necrosis Factor-alpha (metabolism), U118 cells, alzheimer disease, astrocyte, microglia, parkinson disease, s‐aspirin, s‐diclofenac.
- MESH :
- chemical , metabolism : Anti-Inflammatory Agents, Non-Steroidal, Hydrogen Sulfide, Interleukin-6, Nitrites, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Air Pollutants, Anti-Inflammatory Agents, Non-Steroidal, Aspirin, Lipopolysaccharides, Neuroprotective Agents.
- cytology : Temporal Lobe.
- drug effects : Astrocytes, Cell Survival, Intracellular Fluid, Microglia.
- immunology : Astrocytes, Microglia.
- metabolism : Astrocytes, Intracellular Fluid, Microglia.
- Analysis of Variance, Animals, Cells, Cultured, Humans, Time Factors.
Abstract
Endogenously generated hydrogen sulfide (H2S) may have multiple functions in brain. It has been shown that H2S attenuates the expression of pro‐inflammatory cytokines by lipopolysaccharide (LPS)‐activated microglia. Here we demonstrate a neuroprotective effect of NaSH and three H2S‐releasing compounds, ADT‐OH, S‐diclofenac, and S‐aspirin. When activated by LPS and γ‐interferon, human microglia and THP‐1 cells release materials that are toxic to human neuroblastoma SH‐SY5Y cells. These phenomena also occur with γ‐interferon‐stimulated human astroglia and U118 cells. When these cell types are pretreated with aspirin, diclofenac, NASH, or ADT‐OH, the supernatants are significantly less toxic. When they are treated with the NSAID‐H2S hybrid molecules S‐diclofenac and S‐aspirin, which are here referred to as S‐NSAIDs, there is a significant enhancement of the protection. The effect is concentration and incubation time dependent. Such pretreatment also reduces the release of the proinflammatory mediators TNFα, IL‐6, and nitric oxide. The H2S‐releasing compounds are without effect when applied directly to SH‐SY5Y cells. These data suggest that hybrid H2S releasing compounds have significant antiinflammatory properties and may be candidates for treating neurodegenerative disorders that have a prominent neuroinflammatory component such as Alzheimer disease and Parkinson disease. © 2009 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/glia.20905
Affiliations:
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Mcgeer</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC</wicri:regionArea><wicri:noRegion>BC</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Glia</title><title level="j" type="abbrev">Glia</title><idno type="ISSN">0894-1491</idno><idno type="eISSN">1098-1136</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-01-01">2010-01-01</date><biblScope unit="volume">58</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="103">103</biblScope><biblScope unit="page" to="113">113</biblScope></imprint><idno type="ISSN">0894-1491</idno></series><idno type="istex">C1B8E3C396D7B7D9F981A7243358066FFAC6D488</idno><idno type="DOI">10.1002/glia.20905</idno><idno type="ArticleID">GLIA20905</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0894-1491</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Air Pollutants (pharmacology)</term><term>Analysis of Variance</term><term>Animals</term><term>Anti-Inflammatory Agents, Non-Steroidal (metabolism)</term><term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term><term>Aspirin (pharmacology)</term><term>Astrocytes (drug effects)</term><term>Astrocytes (immunology)</term><term>Astrocytes (metabolism)</term><term>Cell Survival (drug effects)</term><term>Cells, Cultured</term><term>Humans</term><term>Hydrogen Sulfide (metabolism)</term><term>Interleukin-6 (metabolism)</term><term>Intracellular Fluid (drug effects)</term><term>Intracellular Fluid (metabolism)</term><term>Lipopolysaccharides (pharmacology)</term><term>Microglia (drug effects)</term><term>Microglia (immunology)</term><term>Microglia (metabolism)</term><term>Neuroprotective Agents (pharmacology)</term><term>Nitrites (metabolism)</term><term>THP‐1 cells</term><term>Temporal Lobe (cytology)</term><term>Time Factors</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>U118 cells</term><term>alzheimer disease</term><term>astrocyte</term><term>microglia</term><term>parkinson disease</term><term>s‐aspirin</term><term>s‐diclofenac</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Hydrogen Sulfide</term><term>Interleukin-6</term><term>Nitrites</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Air Pollutants</term><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Aspirin</term><term>Lipopolysaccharides</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Astrocytes</term><term>Cell Survival</term><term>Intracellular Fluid</term><term>Microglia</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Astrocytes</term><term>Microglia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Intracellular Fluid</term><term>Microglia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Cells, Cultured</term><term>Humans</term><term>Time Factors</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Endogenously generated hydrogen sulfide (H2S) may have multiple functions in brain. It has been shown that H2S attenuates the expression of pro‐inflammatory cytokines by lipopolysaccharide (LPS)‐activated microglia. Here we demonstrate a neuroprotective effect of NaSH and three H2S‐releasing compounds, ADT‐OH, S‐diclofenac, and S‐aspirin. When activated by LPS and γ‐interferon, human microglia and THP‐1 cells release materials that are toxic to human neuroblastoma SH‐SY5Y cells. These phenomena also occur with γ‐interferon‐stimulated human astroglia and U118 cells. When these cell types are pretreated with aspirin, diclofenac, NASH, or ADT‐OH, the supernatants are significantly less toxic. When they are treated with the NSAID‐H2S hybrid molecules S‐diclofenac and S‐aspirin, which are here referred to as S‐NSAIDs, there is a significant enhancement of the protection. The effect is concentration and incubation time dependent. Such pretreatment also reduces the release of the proinflammatory mediators TNFα, IL‐6, and nitric oxide. The H2S‐releasing compounds are without effect when applied directly to SH‐SY5Y cells. These data suggest that hybrid H2S releasing compounds have significant antiinflammatory properties and may be candidates for treating neurodegenerative disorders that have a prominent neuroinflammatory component such as Alzheimer disease and Parkinson disease. © 2009 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Canada</li><li>Italie</li></country><region><li>Lombardie</li></region><settlement><li>Milan</li></settlement></list><tree><country name="Canada"><noRegion><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name></noRegion><name sortKey="Mcgeer, Edith" sort="Mcgeer, Edith" uniqKey="Mcgeer E" first="Edith" last="Mcgeer">Edith Mcgeer</name><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name></country><country name="Italie"><region name="Lombardie"><name sortKey="Sparatore, Anna" sort="Sparatore, Anna" uniqKey="Sparatore A" first="Anna" last="Sparatore">Anna Sparatore</name></region><name sortKey="Del Soldato, Piero" sort="Del Soldato, Piero" uniqKey="Del Soldato P" first="Piero" last="Del Soldato">Piero Del Soldato</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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