Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity
Parkinson’s disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2015-01, Vol.2015 (2015), p.1-6 |
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| creator | Guevara, J. Gómez, C. Rubio, C. Pérez-Severiano, F. Montes, Sergio Gorostieta-Salas, E. Rubio-Osornio, M. Ríos, Camilo |
| description | Parkinson’s disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P |
| doi_str_mv | 10.1155/2015/276039 |
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MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P<0.05) the circling MPP+-induced behavior (10 μg/8 μL). Likewise, EC significantly (P<0.05) reduced the formation of fluorescent lipid products caused by MPP+. MPP+ injection produced (P<0.05) increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P<0.05) reduced as a consequence of MPP+ damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP+. The results show that EC is effective against MPP+-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2015/276039</identifier><identifier>PMID: 26301040</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>1-Methyl-4-phenylpyridinium - toxicity ; Alzheimer's disease ; Animals ; Behavior ; Catechin - metabolism ; Catechin - pharmacology ; Copper - metabolism ; Disease Models, Animal ; Dopamine ; Flavonoids ; Free radicals ; Lipids ; Male ; Neurotoxicity ; Oxidative stress ; Polyphenols ; Rats ; Rats, Wistar ; Rodents ; Zinc - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2015-01, Vol.2015 (2015), p.1-6</ispartof><rights>Copyright © 2015 M. Rubio-Osornio et al.</rights><rights>Copyright © 2015 M. Rubio-Osornio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2015 M. Rubio-Osornio et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-abc4ccd7f9ede4c73423d4c845ecb5bd63f1af29cce9448866051d1c730ec5533</citedby><cites>FETCH-LOGICAL-c467t-abc4ccd7f9ede4c73423d4c845ecb5bd63f1af29cce9448866051d1c730ec5533</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/PMC4537749/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537749/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26301040$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Korrapati, Sathyasaikumar V.</contributor><creatorcontrib>Guevara, J.</creatorcontrib><creatorcontrib>Gómez, C.</creatorcontrib><creatorcontrib>Rubio, C.</creatorcontrib><creatorcontrib>Pérez-Severiano, F.</creatorcontrib><creatorcontrib>Montes, Sergio</creatorcontrib><creatorcontrib>Gorostieta-Salas, E.</creatorcontrib><creatorcontrib>Rubio-Osornio, M.</creatorcontrib><creatorcontrib>Ríos, Camilo</creatorcontrib><title>Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Parkinson’s disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P<0.05) the circling MPP+-induced behavior (10 μg/8 μL). Likewise, EC significantly (P<0.05) reduced the formation of fluorescent lipid products caused by MPP+. MPP+ injection produced (P<0.05) increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P<0.05) reduced as a consequence of MPP+ damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP+. The results show that EC is effective against MPP+-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.</description><subject>1-Methyl-4-phenylpyridinium - toxicity</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Behavior</subject><subject>Catechin - metabolism</subject><subject>Catechin - pharmacology</subject><subject>Copper - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Flavonoids</subject><subject>Free radicals</subject><subject>Lipids</subject><subject>Male</subject><subject>Neurotoxicity</subject><subject>Oxidative stress</subject><subject>Polyphenols</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Zinc - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0c1rFDEYBvBBFFurJ-8S8CLW0WTyNbkIZfvhQqXF1YuXkE3emUmZndkmmUr_ezNsXaonL0lIfnlIeIriNcEfCeH8U4VJHqTAVD0pDoliVYmVYk_3a4wPihcx3mAsaMXI8-KgEhQTzPBh0Z5tvTUJbOcH9A3cZCGiVQreJNOjr9fXx-VymHcdOjUb0wKanUkRpS6MU9uhVe_bLqHlYAOYmG9nsLo6LRfTh58DOrHJ3_l0_7J41pg-wquH-aj4cX72ffGlvLy6WC5OLkvLhEylWVtmrZONAgfMSsoq6pitGQe75msnaENMUylrQTFW10JgThzJEIPlnNKj4vMudzutN-AsDCmYXm-D35hwr0fj9d8ng-90O95pxqmUTOWAdw8BYbydICa98dFC35sBxilqIrHgsq7rKtO3_9CbcQpD_t6sFBN1tlkd75QNY4wBmv1jCNZzgXouUO8KzPrN4_fv7Z_GMni_A7kwZ375_0uDTKAxj7DkXEr6GxzErEo</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Guevara, J.</creator><creator>Gómez, C.</creator><creator>Rubio, C.</creator><creator>Pérez-Severiano, F.</creator><creator>Montes, Sergio</creator><creator>Gorostieta-Salas, E.</creator><creator>Rubio-Osornio, M.</creator><creator>Ríos, Camilo</creator><general>Hindawi Publishing Corporation</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150101</creationdate><title>Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity</title><author>Guevara, J. ; 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MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P<0.05) the circling MPP+-induced behavior (10 μg/8 μL). Likewise, EC significantly (P<0.05) reduced the formation of fluorescent lipid products caused by MPP+. MPP+ injection produced (P<0.05) increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P<0.05) reduced as a consequence of MPP+ damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP+. The results show that EC is effective against MPP+-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26301040</pmid><doi>10.1155/2015/276039</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Methyl-4-phenylpyridinium - toxicity Alzheimer's disease Animals Behavior Catechin - metabolism Catechin - pharmacology Copper - metabolism Disease Models, Animal Dopamine Flavonoids Free radicals Lipids Male Neurotoxicity Oxidative stress Polyphenols Rats Rats, Wistar Rodents Zinc - metabolism |
| title | Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity |
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