The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo
Brain inflammatory processes underlie the pathogenesis of Alzheimer’s disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cycloo...
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| Veröffentlicht in: | Neuroscience 2003-01, Vol.117 (4), p.909-919 |
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| creator | Scali, C Giovannini, M.G Prosperi, C Bellucci, A Pepeu, G Casamenti, F |
| description | Brain inflammatory processes underlie the pathogenesis of Alzheimer’s disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study
in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cyclooxygenase-2 inhibitor, rofecoxib, may prevent neurodegeneration, as a contribution to a better understanding of the role inflammation plays in the pathology of Alzheimer’s disease. We investigated, by immunohistochemical methods, glia reaction, the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway with an antibody selective for the phosphorylated form of the enzyme and the number of choline acetyltransferase-positive neurons and, by
in vivo microdialysis, cortical extracellular levels of acetylcholine following the injection of quisqualic acid into the right nucleus basalis of adult rats. Seven days after injection, a marked reduction in the number of choline acetyltransferase-positive neurons was found, along with an intense glia reaction, selective activation of p38MAPK at the injection site and a significant decrease in the extracellular levels of acetylcholine in the cortex ipsilateral to the injection site. The loss of cholinergic neurons persisted for at least up to 28 days. Rofecoxib (3 mg/kg/day, starting 1 h prior to injection of quisqualic acid) treatment for 7 days significantly attenuated glia activation and prevented the loss of choline acetyltransferase-positive cells and a decrease in cortical acetylcholine release. The prevention of cholinergic cell loss by rofecoxib occurred concomitantly with the inhibition of p38MAPK phosphorylation. Our findings suggest an important role of brain inflammatory reaction in cholinergic degeneration and demonstrate a neuroprotective effect of rofecoxib, presumably mediated through the inhibition of p38MAPK phosphorylation. |
| doi_str_mv | 10.1016/S0306-4522(02)00839-4 |
| format | Article |
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in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cyclooxygenase-2 inhibitor, rofecoxib, may prevent neurodegeneration, as a contribution to a better understanding of the role inflammation plays in the pathology of Alzheimer’s disease. We investigated, by immunohistochemical methods, glia reaction, the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway with an antibody selective for the phosphorylated form of the enzyme and the number of choline acetyltransferase-positive neurons and, by
in vivo microdialysis, cortical extracellular levels of acetylcholine following the injection of quisqualic acid into the right nucleus basalis of adult rats. Seven days after injection, a marked reduction in the number of choline acetyltransferase-positive neurons was found, along with an intense glia reaction, selective activation of p38MAPK at the injection site and a significant decrease in the extracellular levels of acetylcholine in the cortex ipsilateral to the injection site. The loss of cholinergic neurons persisted for at least up to 28 days. Rofecoxib (3 mg/kg/day, starting 1 h prior to injection of quisqualic acid) treatment for 7 days significantly attenuated glia activation and prevented the loss of choline acetyltransferase-positive cells and a decrease in cortical acetylcholine release. The prevention of cholinergic cell loss by rofecoxib occurred concomitantly with the inhibition of p38MAPK phosphorylation. Our findings suggest an important role of brain inflammatory reaction in cholinergic degeneration and demonstrate a neuroprotective effect of rofecoxib, presumably mediated through the inhibition of p38MAPK phosphorylation.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/S0306-4522(02)00839-4</identifier><identifier>PMID: 12654342</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Alzheimer Disease - drug therapy ; Alzheimer Disease - enzymology ; Alzheimer Disease - physiopathology ; Animals ; Astrocytes - drug effects ; Astrocytes - enzymology ; Biological and medical sciences ; Brain - drug effects ; Brain - enzymology ; Brain - physiopathology ; Cell Death - drug effects ; Cell Death - physiology ; Choline O-Acetyltransferase - drug effects ; Choline O-Acetyltransferase - metabolism ; cholinergic degeneration ; Cholinergic Fibers - drug effects ; Cholinergic Fibers - enzymology ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors - pharmacology ; Encephalitis - drug therapy ; Encephalitis - enzymology ; Encephalitis - physiopathology ; glia reactivity ; Gliosis - drug therapy ; Gliosis - enzymology ; Gliosis - prevention & control ; Isoenzymes - antagonists & inhibitors ; Isoenzymes - metabolism ; Lactones - pharmacology ; Male ; Medical sciences ; Microglia - drug effects ; Microglia - enzymology ; Mitogen-Activated Protein Kinases - drug effects ; Mitogen-Activated Protein Kinases - metabolism ; Nerve Degeneration - drug therapy ; Nerve Degeneration - enzymology ; Nerve Degeneration - prevention & control ; Neurons - drug effects ; Neurons - enzymology ; Neuropharmacology ; Neuroprotective agent ; Neuroprotective Agents - pharmacology ; Neurotoxins - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases ; p38-mitogen-activated protein kinase ; Pharmacology. Drug treatments ; Phosphorylation - drug effects ; Prostaglandin-Endoperoxide Synthases - metabolism ; quisqualic acid ; Quisqualic Acid - antagonists & inhibitors ; rat ; Rats ; Rats, Wistar ; rofecoxib ; Sulfones</subject><ispartof>Neuroscience, 2003-01, Vol.117 (4), p.909-919</ispartof><rights>2003 IBRO</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-1db1637b3f3ff0614d22cee3c533dc1069d73ab5409d5ed85ab38f44b39f44f63</citedby><cites>FETCH-LOGICAL-c474t-1db1637b3f3ff0614d22cee3c533dc1069d73ab5409d5ed85ab38f44b39f44f63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0306-4522(02)00839-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14655909$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12654342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Scali, C</creatorcontrib><creatorcontrib>Giovannini, M.G</creatorcontrib><creatorcontrib>Prosperi, C</creatorcontrib><creatorcontrib>Bellucci, A</creatorcontrib><creatorcontrib>Pepeu, G</creatorcontrib><creatorcontrib>Casamenti, F</creatorcontrib><title>The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Brain inflammatory processes underlie the pathogenesis of Alzheimer’s disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study
in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cyclooxygenase-2 inhibitor, rofecoxib, may prevent neurodegeneration, as a contribution to a better understanding of the role inflammation plays in the pathology of Alzheimer’s disease. We investigated, by immunohistochemical methods, glia reaction, the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway with an antibody selective for the phosphorylated form of the enzyme and the number of choline acetyltransferase-positive neurons and, by
in vivo microdialysis, cortical extracellular levels of acetylcholine following the injection of quisqualic acid into the right nucleus basalis of adult rats. Seven days after injection, a marked reduction in the number of choline acetyltransferase-positive neurons was found, along with an intense glia reaction, selective activation of p38MAPK at the injection site and a significant decrease in the extracellular levels of acetylcholine in the cortex ipsilateral to the injection site. The loss of cholinergic neurons persisted for at least up to 28 days. Rofecoxib (3 mg/kg/day, starting 1 h prior to injection of quisqualic acid) treatment for 7 days significantly attenuated glia activation and prevented the loss of choline acetyltransferase-positive cells and a decrease in cortical acetylcholine release. The prevention of cholinergic cell loss by rofecoxib occurred concomitantly with the inhibition of p38MAPK phosphorylation. Our findings suggest an important role of brain inflammatory reaction in cholinergic degeneration and demonstrate a neuroprotective effect of rofecoxib, presumably mediated through the inhibition of p38MAPK phosphorylation.</description><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - enzymology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Animals</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - enzymology</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - enzymology</subject><subject>Brain - physiopathology</subject><subject>Cell Death - drug effects</subject><subject>Cell Death - physiology</subject><subject>Choline O-Acetyltransferase - drug effects</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>cholinergic degeneration</subject><subject>Cholinergic Fibers - drug effects</subject><subject>Cholinergic Fibers - enzymology</subject><subject>Cyclooxygenase 2</subject><subject>Cyclooxygenase 2 Inhibitors</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Encephalitis - drug therapy</subject><subject>Encephalitis - enzymology</subject><subject>Encephalitis - physiopathology</subject><subject>glia reactivity</subject><subject>Gliosis - drug therapy</subject><subject>Gliosis - enzymology</subject><subject>Gliosis - prevention & control</subject><subject>Isoenzymes - antagonists & inhibitors</subject><subject>Isoenzymes - metabolism</subject><subject>Lactones - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microglia - drug effects</subject><subject>Microglia - enzymology</subject><subject>Mitogen-Activated Protein Kinases - drug effects</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Nerve Degeneration - drug therapy</subject><subject>Nerve Degeneration - enzymology</subject><subject>Nerve Degeneration - prevention & control</subject><subject>Neurons - drug effects</subject><subject>Neurons - enzymology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neurotoxins - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>p38-mitogen-activated protein kinase</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation - drug effects</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>quisqualic acid</subject><subject>Quisqualic Acid - antagonists & inhibitors</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>rofecoxib</subject><subject>Sulfones</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9uEzEQxi0EomnhEUC-gOCwxV7b--eEUEUBqVIPLWfLa48bo107eHaj5El43Tokokcsy-PDb74ZfR8hbzi75Iw3n-6YYE0lVV1_YPVHxjrRV_IZWfGuFVWrpHxOVv-QM3KO-IuVo6R4Sc543ZSPrFfkz_0aKMIIdg5boHZvx5R2-weIBqGqaYjrMIQ5ZZqTB5t2YaC4bDYZEAHpkE2IBfKjmSYzhxSpiY5ucpqLIlK7TmOIkB-CpRGWnCJSn9NEYWeL6lz0LHVQxkE-the5bdimV-SFNyPC61O9ID-vv95ffa9ubr_9uPpyU1nZyrnibuCNaAfhhfes4dLVtQUQVgnhLGdN71phBiVZ7xS4TplBdF7KQfTl9Y24IO-PumXl3wvgrKeAFsbRREgLat71vOeMFVAdQZsTYgavNzlMJu81Z_qQiP6biD7YrVm5h0S0LH1vTwOWYQL31HWKoADvToBBa0afTbQBnzjZKNWzvnCfjxwUO7YBskYbIFpwIRevtUvhP6s8At-OrK8</recordid><startdate>20030101</startdate><enddate>20030101</enddate><creator>Scali, C</creator><creator>Giovannini, M.G</creator><creator>Prosperi, C</creator><creator>Bellucci, A</creator><creator>Pepeu, G</creator><creator>Casamenti, F</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20030101</creationdate><title>The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo</title><author>Scali, C ; Giovannini, M.G ; Prosperi, C ; Bellucci, A ; Pepeu, G ; Casamenti, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-1db1637b3f3ff0614d22cee3c533dc1069d73ab5409d5ed85ab38f44b39f44f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - enzymology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Animals</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - enzymology</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - enzymology</topic><topic>Brain - physiopathology</topic><topic>Cell Death - drug effects</topic><topic>Cell Death - physiology</topic><topic>Choline O-Acetyltransferase - drug effects</topic><topic>Choline O-Acetyltransferase - metabolism</topic><topic>cholinergic degeneration</topic><topic>Cholinergic Fibers - drug effects</topic><topic>Cholinergic Fibers - enzymology</topic><topic>Cyclooxygenase 2</topic><topic>Cyclooxygenase 2 Inhibitors</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Encephalitis - drug therapy</topic><topic>Encephalitis - enzymology</topic><topic>Encephalitis - physiopathology</topic><topic>glia reactivity</topic><topic>Gliosis - drug therapy</topic><topic>Gliosis - enzymology</topic><topic>Gliosis - prevention & control</topic><topic>Isoenzymes - antagonists & inhibitors</topic><topic>Isoenzymes - metabolism</topic><topic>Lactones - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microglia - drug effects</topic><topic>Microglia - enzymology</topic><topic>Mitogen-Activated Protein Kinases - drug effects</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Nerve Degeneration - drug therapy</topic><topic>Nerve Degeneration - enzymology</topic><topic>Nerve Degeneration - prevention & control</topic><topic>Neurons - drug effects</topic><topic>Neurons - enzymology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neurotoxins - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>p38-mitogen-activated protein kinase</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation - drug effects</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>quisqualic acid</topic><topic>Quisqualic Acid - antagonists & inhibitors</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>rofecoxib</topic><topic>Sulfones</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Scali, C</creatorcontrib><creatorcontrib>Giovannini, M.G</creatorcontrib><creatorcontrib>Prosperi, C</creatorcontrib><creatorcontrib>Bellucci, A</creatorcontrib><creatorcontrib>Pepeu, G</creatorcontrib><creatorcontrib>Casamenti, F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Scali, C</au><au>Giovannini, M.G</au><au>Prosperi, C</au><au>Bellucci, A</au><au>Pepeu, G</au><au>Casamenti, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2003-01-01</date><risdate>2003</risdate><volume>117</volume><issue>4</issue><spage>909</spage><epage>919</epage><pages>909-919</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Brain inflammatory processes underlie the pathogenesis of Alzheimer’s disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study
in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cyclooxygenase-2 inhibitor, rofecoxib, may prevent neurodegeneration, as a contribution to a better understanding of the role inflammation plays in the pathology of Alzheimer’s disease. We investigated, by immunohistochemical methods, glia reaction, the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway with an antibody selective for the phosphorylated form of the enzyme and the number of choline acetyltransferase-positive neurons and, by
in vivo microdialysis, cortical extracellular levels of acetylcholine following the injection of quisqualic acid into the right nucleus basalis of adult rats. Seven days after injection, a marked reduction in the number of choline acetyltransferase-positive neurons was found, along with an intense glia reaction, selective activation of p38MAPK at the injection site and a significant decrease in the extracellular levels of acetylcholine in the cortex ipsilateral to the injection site. The loss of cholinergic neurons persisted for at least up to 28 days. Rofecoxib (3 mg/kg/day, starting 1 h prior to injection of quisqualic acid) treatment for 7 days significantly attenuated glia activation and prevented the loss of choline acetyltransferase-positive cells and a decrease in cortical acetylcholine release. The prevention of cholinergic cell loss by rofecoxib occurred concomitantly with the inhibition of p38MAPK phosphorylation. Our findings suggest an important role of brain inflammatory reaction in cholinergic degeneration and demonstrate a neuroprotective effect of rofecoxib, presumably mediated through the inhibition of p38MAPK phosphorylation.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12654342</pmid><doi>10.1016/S0306-4522(02)00839-4</doi><tpages>11</tpages></addata></record> |
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| ispartof | Neuroscience, 2003-01, Vol.117 (4), p.909-919 |
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| subjects | Alzheimer Disease - drug therapy Alzheimer Disease - enzymology Alzheimer Disease - physiopathology Animals Astrocytes - drug effects Astrocytes - enzymology Biological and medical sciences Brain - drug effects Brain - enzymology Brain - physiopathology Cell Death - drug effects Cell Death - physiology Choline O-Acetyltransferase - drug effects Choline O-Acetyltransferase - metabolism cholinergic degeneration Cholinergic Fibers - drug effects Cholinergic Fibers - enzymology Cyclooxygenase 2 Cyclooxygenase 2 Inhibitors Cyclooxygenase Inhibitors - pharmacology Encephalitis - drug therapy Encephalitis - enzymology Encephalitis - physiopathology glia reactivity Gliosis - drug therapy Gliosis - enzymology Gliosis - prevention & control Isoenzymes - antagonists & inhibitors Isoenzymes - metabolism Lactones - pharmacology Male Medical sciences Microglia - drug effects Microglia - enzymology Mitogen-Activated Protein Kinases - drug effects Mitogen-Activated Protein Kinases - metabolism Nerve Degeneration - drug therapy Nerve Degeneration - enzymology Nerve Degeneration - prevention & control Neurons - drug effects Neurons - enzymology Neuropharmacology Neuroprotective agent Neuroprotective Agents - pharmacology Neurotoxins - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases p38-mitogen-activated protein kinase Pharmacology. Drug treatments Phosphorylation - drug effects Prostaglandin-Endoperoxide Synthases - metabolism quisqualic acid Quisqualic Acid - antagonists & inhibitors rat Rats Rats, Wistar rofecoxib Sulfones |
| title | The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo |
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