Neuroprotective effects of the triterpenoid, CDDO methyl amide, a potent inducer of Nrf2-mediated transcription
The NF-E2-related factor-2 (Nrf2)/antioxidant response element (ARE) signaling pathway regulates phase 2 detoxification genes, including a variety of antioxidative enzymes. We tested neuroprotective effects of the synthetic triterpenoid CDDO-MA, a potent activator of the Nrf2/ARE signaling. CDDO-MA...
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creator | Yang, Lichuan Calingasan, Noel Y Thomas, Bobby Chaturvedi, Rajnish K Kiaei, Mahmoud Wille, Elizabeth J Liby, Karen T Williams, Charlotte Royce, Darlene Risingsong, Renee Musiek, Eric S Morrow, Jason D Sporn, Michael Beal, M Flint |
description | The NF-E2-related factor-2 (Nrf2)/antioxidant response element (ARE) signaling pathway regulates phase 2 detoxification genes, including a variety of antioxidative enzymes. We tested neuroprotective effects of the synthetic triterpenoid CDDO-MA, a potent activator of the Nrf2/ARE signaling. CDDO-MA treatment of neuroblastoma SH-SY5Y cells resulted in Nrf2 upregulation and translocation from cytosol to nucleus and subsequent activation of ARE pathway genes. CDDO-MA blocked t-butylhydroperoxide-induced production of reactive oxygen species (ROS) by activation of ARE genes only in wild type, but not Nrf2 knockout mouse embryonic fibroblasts. Oral administration of CDDO-MA resulted in significant protection against MPTP-induced nigrostriatal dopaminergic neurodegeneration, pathological alpha-synuclein accumulation and oxidative damage in mice. Additionally, CDDO-MA treatment in rats produced significant rescue against striatal lesions caused by the neurotoxin 3-NP, and associated increases in the oxidative damage markers malondialdehyde, F(2)-Isoprostanes, 8-hydroxy-2-deoxyguanosine, 3-nitrotyrosine, and impaired glutathione homeostasis. Our results indicate that the CDDO-MA renders its neuroprotective effects through its potent activation of the Nrf2/ARE pathway, and suggest that triterpenoids may be beneficial for the treatment of neurodegenerative diseases like Parkinson's disease and Huntington's disease. |
doi_str_mv | 10.1371/journal.pone.0005757 |
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We tested neuroprotective effects of the synthetic triterpenoid CDDO-MA, a potent activator of the Nrf2/ARE signaling. CDDO-MA treatment of neuroblastoma SH-SY5Y cells resulted in Nrf2 upregulation and translocation from cytosol to nucleus and subsequent activation of ARE pathway genes. CDDO-MA blocked t-butylhydroperoxide-induced production of reactive oxygen species (ROS) by activation of ARE genes only in wild type, but not Nrf2 knockout mouse embryonic fibroblasts. Oral administration of CDDO-MA resulted in significant protection against MPTP-induced nigrostriatal dopaminergic neurodegeneration, pathological alpha-synuclein accumulation and oxidative damage in mice. Additionally, CDDO-MA treatment in rats produced significant rescue against striatal lesions caused by the neurotoxin 3-NP, and associated increases in the oxidative damage markers malondialdehyde, F(2)-Isoprostanes, 8-hydroxy-2-deoxyguanosine, 3-nitrotyrosine, and impaired glutathione homeostasis. Our results indicate that the CDDO-MA renders its neuroprotective effects through its potent activation of the Nrf2/ARE pathway, and suggest that triterpenoids may be beneficial for the treatment of neurodegenerative diseases like Parkinson's disease and Huntington's disease.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0005757</identifier><identifier>PMID: 19484125</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Alzheimer's disease ; Alzheimers disease ; Analysis ; Animals ; Antifungal agents ; Antioxidants ; Antioxidants (Nutrients) ; Antioxidants - metabolism ; Cell Line, Tumor ; Chemical compounds ; Chromatography ; Cytosol ; Damage accumulation ; Deoxyguanosine ; Deoxyribonucleic acid ; Detoxification ; DNA ; DNA polymerase ; Dopamine ; Dopamine receptors ; Embryo fibroblasts ; Embryos ; Enzymes ; Fibroblasts ; Gene expression ; Genes ; Glutathione ; Homeostasis ; Hospitals ; Humans ; Huntington's disease ; Isoprostanes ; Lesions ; Male ; Malondialdehyde ; Medical schools ; Medical treatment ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Movement disorders ; MPTP ; Neostriatum ; Nervous system diseases ; Neurodegeneration ; Neurodegenerative diseases ; Neurodegenerative Diseases - pathology ; Neurological diseases ; Neurological Disorders ; Neurological Disorders/Alzheimer Disease ; Neurological Disorders/Movement Disorders ; Neurological Disorders/Neuropharmacology ; Neurology ; Neuroprotection ; Neuroscience ; Neuroscience/Motor Systems ; Neurosciences ; Neurotoxicity ; Neurotoxins ; NF-E2-Related Factor 2 - metabolism ; Nitrotyrosine ; Nuclei (cytology) ; Oleanolic Acid - analogs & derivatives ; Oleanolic Acid - pharmacokinetics ; Oleanolic Acid - pharmacology ; Oral administration ; Oxygen ; Parkinson's disease ; Pharmacology ; Polymerase chain reaction ; Proteins ; Rats ; Rats, Inbred Lew ; Reactive oxygen species ; Rodents ; Signal transduction ; Signaling ; Synuclein ; Terpenes - metabolism ; Thermus aquaticus ; Transcription (Genetics) ; Transcription, Genetic ; Translocation</subject><ispartof>PloS one, 2009-06, Vol.4 (6), p.e5757-e5757</ispartof><rights>COPYRIGHT 2009 Public Library of Science</rights><rights>2009 Yang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Yang et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c759t-8943e721607af220db7d0963061b52ed6fe653749e4b5dbc4ac0460eba6cbc2c3</citedby><cites>FETCH-LOGICAL-c759t-8943e721607af220db7d0963061b52ed6fe653749e4b5dbc4ac0460eba6cbc2c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684590/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684590/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23847,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19484125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gendelman, Howard E.</contributor><creatorcontrib>Yang, Lichuan</creatorcontrib><creatorcontrib>Calingasan, Noel Y</creatorcontrib><creatorcontrib>Thomas, Bobby</creatorcontrib><creatorcontrib>Chaturvedi, Rajnish K</creatorcontrib><creatorcontrib>Kiaei, Mahmoud</creatorcontrib><creatorcontrib>Wille, Elizabeth J</creatorcontrib><creatorcontrib>Liby, Karen T</creatorcontrib><creatorcontrib>Williams, Charlotte</creatorcontrib><creatorcontrib>Royce, Darlene</creatorcontrib><creatorcontrib>Risingsong, Renee</creatorcontrib><creatorcontrib>Musiek, Eric S</creatorcontrib><creatorcontrib>Morrow, Jason D</creatorcontrib><creatorcontrib>Sporn, Michael</creatorcontrib><creatorcontrib>Beal, M Flint</creatorcontrib><title>Neuroprotective effects of the triterpenoid, CDDO methyl amide, a potent inducer of Nrf2-mediated transcription</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The NF-E2-related factor-2 (Nrf2)/antioxidant response element (ARE) signaling pathway regulates phase 2 detoxification genes, including a variety of antioxidative enzymes. We tested neuroprotective effects of the synthetic triterpenoid CDDO-MA, a potent activator of the Nrf2/ARE signaling. CDDO-MA treatment of neuroblastoma SH-SY5Y cells resulted in Nrf2 upregulation and translocation from cytosol to nucleus and subsequent activation of ARE pathway genes. CDDO-MA blocked t-butylhydroperoxide-induced production of reactive oxygen species (ROS) by activation of ARE genes only in wild type, but not Nrf2 knockout mouse embryonic fibroblasts. Oral administration of CDDO-MA resulted in significant protection against MPTP-induced nigrostriatal dopaminergic neurodegeneration, pathological alpha-synuclein accumulation and oxidative damage in mice. Additionally, CDDO-MA treatment in rats produced significant rescue against striatal lesions caused by the neurotoxin 3-NP, and associated increases in the oxidative damage markers malondialdehyde, F(2)-Isoprostanes, 8-hydroxy-2-deoxyguanosine, 3-nitrotyrosine, and impaired glutathione homeostasis. Our results indicate that the CDDO-MA renders its neuroprotective effects through its potent activation of the Nrf2/ARE pathway, and suggest that triterpenoids may be beneficial for the treatment of neurodegenerative diseases like Parkinson's disease and Huntington's disease.</description><subject>Activation</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Analysis</subject><subject>Animals</subject><subject>Antifungal agents</subject><subject>Antioxidants</subject><subject>Antioxidants (Nutrients)</subject><subject>Antioxidants - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Chemical compounds</subject><subject>Chromatography</subject><subject>Cytosol</subject><subject>Damage accumulation</subject><subject>Deoxyguanosine</subject><subject>Deoxyribonucleic acid</subject><subject>Detoxification</subject><subject>DNA</subject><subject>DNA polymerase</subject><subject>Dopamine</subject><subject>Dopamine receptors</subject><subject>Embryo fibroblasts</subject><subject>Embryos</subject><subject>Enzymes</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Glutathione</subject><subject>Homeostasis</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Huntington's disease</subject><subject>Isoprostanes</subject><subject>Lesions</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Medical schools</subject><subject>Medical treatment</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Models, Biological</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>Neostriatum</subject><subject>Nervous system diseases</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurodegenerative Diseases - pathology</subject><subject>Neurological diseases</subject><subject>Neurological Disorders</subject><subject>Neurological Disorders/Alzheimer Disease</subject><subject>Neurological Disorders/Movement Disorders</subject><subject>Neurological Disorders/Neuropharmacology</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroscience</subject><subject>Neuroscience/Motor Systems</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Neurotoxins</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nitrotyrosine</subject><subject>Nuclei (cytology)</subject><subject>Oleanolic Acid - analogs & derivatives</subject><subject>Oleanolic Acid - pharmacokinetics</subject><subject>Oleanolic Acid - pharmacology</subject><subject>Oral administration</subject><subject>Oxygen</subject><subject>Parkinson's disease</subject><subject>Pharmacology</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Synuclein</subject><subject>Terpenes - metabolism</subject><subject>Thermus aquaticus</subject><subject>Transcription (Genetics)</subject><subject>Transcription, Genetic</subject><subject>Translocation</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAYhYso7rr6D0QLwoKwMyZpmrQ3wjLrx8CyA37dhjR5M5OhbbpJurj_3oxTdUa8kFwkpM856Xs4WfYcozkuOH6zdaPvZTsfXA9zhFDJS_4gO8V1QWaMoOLhwfkkexLCNjFFxdjj7ATXtKKYlKeZu4HRu8G7CCraO8jBmHQKuTN53EAevY3gB-id1Rf54upqlXcQN_dtLjur4SKX-ZC0fcxtr0cFfie88YbMOtBWRtDJQvZBeTtE6_qn2SMj2wDPpv0s-_r-3ZfFx9n16sNycXk9U7ys46yqaQGcYIa4NIQg3XCNalYghpuSgGYGWFlwWgNtSt0oKhWiDEEjmWoUUcVZ9nLvO7QuiCmrIDCpapKioiQRyz2hndyKwdtO-nvhpBU_L5xfC-mjVS0I3iBWalpThRlljak4oRzJitXGVFpVyevt9NrYpLlVysPL9sj0-EtvN2Lt7gRhFS1rlAzOJwPvbkcIUXQ2KGhb2YMbgyAIpVwITeCrv8B_zzbfU2uZft_2xqVXVVoaOqtSYYxN95eUFxjVRVEmwesjQWIifI9rOYYglp8__T-7-nbMnh-wG5Bt3ATXjrsqhGOQ7kHlXQgezO_wMBK7vv-aU-z6Lqa-J9mLw-D_iKaCFz8A2FH8EA</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Yang, Lichuan</creator><creator>Calingasan, Noel Y</creator><creator>Thomas, Bobby</creator><creator>Chaturvedi, Rajnish K</creator><creator>Kiaei, Mahmoud</creator><creator>Wille, Elizabeth J</creator><creator>Liby, Karen T</creator><creator>Williams, Charlotte</creator><creator>Royce, Darlene</creator><creator>Risingsong, Renee</creator><creator>Musiek, Eric S</creator><creator>Morrow, Jason D</creator><creator>Sporn, Michael</creator><creator>Beal, M Flint</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7TK</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20090601</creationdate><title>Neuroprotective effects of the triterpenoid, CDDO methyl amide, a potent inducer of Nrf2-mediated transcription</title><author>Yang, Lichuan ; Calingasan, Noel Y ; Thomas, Bobby ; Chaturvedi, Rajnish K ; Kiaei, Mahmoud ; Wille, Elizabeth J ; Liby, Karen T ; Williams, Charlotte ; Royce, Darlene ; Risingsong, Renee ; Musiek, Eric S ; Morrow, Jason D ; Sporn, Michael ; Beal, M Flint</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c759t-8943e721607af220db7d0963061b52ed6fe653749e4b5dbc4ac0460eba6cbc2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Activation</topic><topic>Alzheimer's disease</topic><topic>Alzheimers disease</topic><topic>Analysis</topic><topic>Animals</topic><topic>Antifungal agents</topic><topic>Antioxidants</topic><topic>Antioxidants (Nutrients)</topic><topic>Antioxidants - 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pathology</topic><topic>Neurological diseases</topic><topic>Neurological Disorders</topic><topic>Neurological Disorders/Alzheimer Disease</topic><topic>Neurological Disorders/Movement Disorders</topic><topic>Neurological Disorders/Neuropharmacology</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroscience</topic><topic>Neuroscience/Motor Systems</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Neurotoxins</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nitrotyrosine</topic><topic>Nuclei (cytology)</topic><topic>Oleanolic Acid - analogs & derivatives</topic><topic>Oleanolic Acid - pharmacokinetics</topic><topic>Oleanolic Acid - pharmacology</topic><topic>Oral administration</topic><topic>Oxygen</topic><topic>Parkinson's disease</topic><topic>Pharmacology</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Synuclein</topic><topic>Terpenes - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Lichuan</au><au>Calingasan, Noel Y</au><au>Thomas, Bobby</au><au>Chaturvedi, Rajnish K</au><au>Kiaei, Mahmoud</au><au>Wille, Elizabeth J</au><au>Liby, Karen T</au><au>Williams, Charlotte</au><au>Royce, Darlene</au><au>Risingsong, Renee</au><au>Musiek, Eric S</au><au>Morrow, Jason D</au><au>Sporn, Michael</au><au>Beal, M Flint</au><au>Gendelman, Howard E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects of the triterpenoid, CDDO methyl amide, a potent inducer of Nrf2-mediated transcription</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>4</volume><issue>6</issue><spage>e5757</spage><epage>e5757</epage><pages>e5757-e5757</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The NF-E2-related factor-2 (Nrf2)/antioxidant response element (ARE) signaling pathway regulates phase 2 detoxification genes, including a variety of antioxidative enzymes. We tested neuroprotective effects of the synthetic triterpenoid CDDO-MA, a potent activator of the Nrf2/ARE signaling. CDDO-MA treatment of neuroblastoma SH-SY5Y cells resulted in Nrf2 upregulation and translocation from cytosol to nucleus and subsequent activation of ARE pathway genes. CDDO-MA blocked t-butylhydroperoxide-induced production of reactive oxygen species (ROS) by activation of ARE genes only in wild type, but not Nrf2 knockout mouse embryonic fibroblasts. Oral administration of CDDO-MA resulted in significant protection against MPTP-induced nigrostriatal dopaminergic neurodegeneration, pathological alpha-synuclein accumulation and oxidative damage in mice. Additionally, CDDO-MA treatment in rats produced significant rescue against striatal lesions caused by the neurotoxin 3-NP, and associated increases in the oxidative damage markers malondialdehyde, F(2)-Isoprostanes, 8-hydroxy-2-deoxyguanosine, 3-nitrotyrosine, and impaired glutathione homeostasis. Our results indicate that the CDDO-MA renders its neuroprotective effects through its potent activation of the Nrf2/ARE pathway, and suggest that triterpenoids may be beneficial for the treatment of neurodegenerative diseases like Parkinson's disease and Huntington's disease.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>19484125</pmid><doi>10.1371/journal.pone.0005757</doi><tpages>e5757</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2009-06, Vol.4 (6), p.e5757-e5757 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1289205742 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | Activation Alzheimer's disease Alzheimers disease Analysis Animals Antifungal agents Antioxidants Antioxidants (Nutrients) Antioxidants - metabolism Cell Line, Tumor Chemical compounds Chromatography Cytosol Damage accumulation Deoxyguanosine Deoxyribonucleic acid Detoxification DNA DNA polymerase Dopamine Dopamine receptors Embryo fibroblasts Embryos Enzymes Fibroblasts Gene expression Genes Glutathione Homeostasis Hospitals Humans Huntington's disease Isoprostanes Lesions Male Malondialdehyde Medical schools Medical treatment Mice Mice, Inbred C57BL Models, Biological Movement disorders MPTP Neostriatum Nervous system diseases Neurodegeneration Neurodegenerative diseases Neurodegenerative Diseases - pathology Neurological diseases Neurological Disorders Neurological Disorders/Alzheimer Disease Neurological Disorders/Movement Disorders Neurological Disorders/Neuropharmacology Neurology Neuroprotection Neuroscience Neuroscience/Motor Systems Neurosciences Neurotoxicity Neurotoxins NF-E2-Related Factor 2 - metabolism Nitrotyrosine Nuclei (cytology) Oleanolic Acid - analogs & derivatives Oleanolic Acid - pharmacokinetics Oleanolic Acid - pharmacology Oral administration Oxygen Parkinson's disease Pharmacology Polymerase chain reaction Proteins Rats Rats, Inbred Lew Reactive oxygen species Rodents Signal transduction Signaling Synuclein Terpenes - metabolism Thermus aquaticus Transcription (Genetics) Transcription, Genetic Translocation |
title | Neuroprotective effects of the triterpenoid, CDDO methyl amide, a potent inducer of Nrf2-mediated transcription |
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