NOSH‐aspirin (NBS‐1120), a novel nitric oxide and hydrogen sulfide releasing hybrid, attenuates neuroinflammation induced by microglial and astrocytic activation: A new candidate for treatment of neurodegenerative disorders
Identifieur interne : 000F69 ( Main/Exploration ); précédent : 000F68; suivant : 000F70NOSH‐aspirin (NBS‐1120), a novel nitric oxide and hydrogen sulfide releasing hybrid, attenuates neuroinflammation induced by microglial and astrocytic activation: A new candidate for treatment of neurodegenerative disorders
Auteurs : Moonhee Lee [Canada] ; Edith Mcgeer [Canada] ; Ravinder Kodela [États-Unis] ; Khosrow Kashfi [États-Unis] ; Patrick L. Mcgeer [Canada]Source :
- Glia [ 0894-1491 ] ; 2013-10.
English descriptors
- KwdEn :
- Anti-Inflammatory Agents (pharmacology), Aspirin (analogs & derivatives), Aspirin (pharmacology), Astrocytes (drug effects), Astrocytoma (pathology), Cell Line, Tumor, Cells, Cultured, Disulfides (pharmacology), Dose-Response Relationship, Drug, Humans, Interferon-gamma (pharmacology), Interleukin-6 (metabolism), Lipopolysaccharides (pharmacology), Microglia (drug effects), NF-kappa B (metabolism), Nitrates (pharmacology), Signal Transduction (drug effects), Temporal Lobe (cytology), Time Factors, Tumor Necrosis Factor-alpha (metabolism), p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , analogs & derivatives : Aspirin.
- chemical , metabolism : Interleukin-6, NF-kappa B, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Anti-Inflammatory Agents, Aspirin, Disulfides, Interferon-gamma, Lipopolysaccharides, Nitrates.
- cytology : Temporal Lobe.
- drug effects : Astrocytes, Microglia, Signal Transduction.
- pathology : Astrocytoma.
- Cell Line, Tumor, Cells, Cultured, Dose-Response Relationship, Drug, Humans, Time Factors.
Abstract
Hydrogen sulfide (H2S) and nitric oxide (NO) have been described as gasotransmitters. Anti‐inflammatory activity in the central and peripheral nervous systems may be one of their functions. Previously we demonstrated that several SH‐ donors including H2S‐releasing aspirin (S‐ASA) exhibited anti‐inflammatory and neuroprotective activity in vitro against toxins released by activated microglia and astrocytes. Here we report that NOSH‐ASA, an NO‐ and H2S‐releasing hybrid of aspirin, has a significantly greater anti‐inflammatory and neuroprotective effect than S‐ASA or NO‐ASA. When activated by LPS/IFNγ, human microglia and THP‐1 cells release materials that are toxic to differentiated SH‐SY5Y cells. These phenomena also occur with IFNγ‐stimulated human astroglia and U373 cells. When the cells were treated with the S‐ASA or NO‐ASA, there was a significant enhancement of neuroprotection. However, NOSH‐ASA had significantly more potent protection properties than NO‐ASA or S‐ASA. The effect was concentration‐dependent, as well as incubation time‐dependent. Such treatment not only reduced the release of the TNFα and IL‐6, but also attenuated activation of P38 MAPK and NFκB proteins. All the compounds tested were not harmful when applied directly to SH‐SY5Y cells. These data suggest that NOSH‐ASA has significant anti‐inflammatory properties and may be a new candidate for treating neurodegenerative disorders that have a prominent neuroinflammatory component such as Alzheimer disease and Parkinson disease. GLIA 2013;61:1724–1734
Url:
DOI: 10.1002/glia.22553
Affiliations:
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Le document en format XML
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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, BC, V6T 1Z3, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Canada</country></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>Blackwell Publishing Ltd</publisher><date type="published" when="2013-10">2013-10</date><biblScope unit="volume">61</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1724">1724</biblScope><biblScope unit="page" to="1734">1734</biblScope></imprint><idno type="ISSN">0894-1491</idno></series><idno type="istex">B9BD99BC43ADC00231A3187A23F5405E9824283A</idno><idno type="DOI">10.1002/glia.22553</idno><idno type="ArticleID">GLIA22553</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0894-1491</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anti-Inflammatory Agents (pharmacology)</term><term>Aspirin (analogs & derivatives)</term><term>Aspirin (pharmacology)</term><term>Astrocytes (drug effects)</term><term>Astrocytoma (pathology)</term><term>Cell Line, Tumor</term><term>Cells, Cultured</term><term>Disulfides (pharmacology)</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Interferon-gamma (pharmacology)</term><term>Interleukin-6 (metabolism)</term><term>Lipopolysaccharides (pharmacology)</term><term>Microglia (drug effects)</term><term>NF-kappa B (metabolism)</term><term>Nitrates (pharmacology)</term><term>Signal Transduction (drug effects)</term><term>Temporal Lobe (cytology)</term><term>Time Factors</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>p38 Mitogen-Activated Protein Kinases (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspirin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-6</term><term>NF-kappa B</term><term>Tumor Necrosis Factor-alpha</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Aspirin</term><term>Disulfides</term><term>Interferon-gamma</term><term>Lipopolysaccharides</term><term>Nitrates</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>Microglia</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Astrocytoma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Cells, Cultured</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Time Factors</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Hydrogen sulfide (H2S) and nitric oxide (NO) have been described as gasotransmitters. Anti‐inflammatory activity in the central and peripheral nervous systems may be one of their functions. Previously we demonstrated that several SH‐ donors including H2S‐releasing aspirin (S‐ASA) exhibited anti‐inflammatory and neuroprotective activity in vitro against toxins released by activated microglia and astrocytes. Here we report that NOSH‐ASA, an NO‐ and H2S‐releasing hybrid of aspirin, has a significantly greater anti‐inflammatory and neuroprotective effect than S‐ASA or NO‐ASA. When activated by LPS/IFNγ, human microglia and THP‐1 cells release materials that are toxic to differentiated SH‐SY5Y cells. These phenomena also occur with IFNγ‐stimulated human astroglia and U373 cells. When the cells were treated with the S‐ASA or NO‐ASA, there was a significant enhancement of neuroprotection. However, NOSH‐ASA had significantly more potent protection properties than NO‐ASA or S‐ASA. The effect was concentration‐dependent, as well as incubation time‐dependent. Such treatment not only reduced the release of the TNFα and IL‐6, but also attenuated activation of P38 MAPK and NFκB proteins. All the compounds tested were not harmful when applied directly to SH‐SY5Y cells. These data suggest that NOSH‐ASA has significant anti‐inflammatory properties and may be a new candidate for treating neurodegenerative disorders that have a prominent neuroinflammatory component such as Alzheimer disease and Parkinson disease. GLIA 2013;61:1724–1734</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>État de New York</li></region></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="États-Unis"><region name="État de New York"><name sortKey="Kodela, Ravinder" sort="Kodela, Ravinder" uniqKey="Kodela R" first="Ravinder" last="Kodela">Ravinder Kodela</name></region><name sortKey="Kashfi, Khosrow" sort="Kashfi, Khosrow" uniqKey="Kashfi K" first="Khosrow" last="Kashfi">Khosrow Kashfi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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