Quercetin Protects Mouse Brain against Lead-Induced Neurotoxicity
Quercetin (QE), the major bioflavonoid in the human diet, has been reported to have many benefits and medicinal properties. However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxic...
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| Veröffentlicht in: | Journal of agricultural and food chemistry 2013-08, Vol.61 (31), p.7630-7635 |
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| creator | Liu, Chan-Min Zheng, Gui-Hong Cheng, Chao Sun, Jian-Mei |
| description | Quercetin (QE), the major bioflavonoid in the human diet, has been reported to have many benefits and medicinal properties. However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxicity in mice exposed to Pb. Mice were exposed to lead acetate (20 mg/kg body weight/day) intragastrically with or without QE (15 and 30 mg/kg body weight/day) coadministration for 3 months. The data showed that QE significantly prevented Pb-induced neurotoxicity in a dose-dependent manner. Exploration of the underlying mechanisms of QE action revealed that QE administration decreased Pb contents in blood (13.2, 19.1%) and brain (17.1, 20.0%). QE markedly increased NO production (39.1, 61.1%) and PKA activity (51.0, 57.8%) in brains of Pb-treated mice. Additionally, QE remarkably suppressed Pb-induced oxidative stress in mouse brain. Western blot analysis showed that QE increased the phosphorylations of Akt, CaMKII nNOS, eNOS, and CREB in brains of Pb-treated mice. The results suggest that QE can inhibit Pb-induced neurotoxicity and partly restore PKA, Akt, NOS, CaMKII, and CREB activities. |
| doi_str_mv | 10.1021/jf303387d |
| format | Article |
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However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxicity in mice exposed to Pb. Mice were exposed to lead acetate (20 mg/kg body weight/day) intragastrically with or without QE (15 and 30 mg/kg body weight/day) coadministration for 3 months. The data showed that QE significantly prevented Pb-induced neurotoxicity in a dose-dependent manner. Exploration of the underlying mechanisms of QE action revealed that QE administration decreased Pb contents in blood (13.2, 19.1%) and brain (17.1, 20.0%). QE markedly increased NO production (39.1, 61.1%) and PKA activity (51.0, 57.8%) in brains of Pb-treated mice. Additionally, QE remarkably suppressed Pb-induced oxidative stress in mouse brain. Western blot analysis showed that QE increased the phosphorylations of Akt, CaMKII nNOS, eNOS, and CREB in brains of Pb-treated mice. The results suggest that QE can inhibit Pb-induced neurotoxicity and partly restore PKA, Akt, NOS, CaMKII, and CREB activities.</description><identifier>ISSN: 0021-8561</identifier><identifier>EISSN: 1520-5118</identifier><identifier>DOI: 10.1021/jf303387d</identifier><identifier>PMID: 23855546</identifier><identifier>CODEN: JAFCAU</identifier><language>eng</language><publisher>Washington, DC: American Chemical Society</publisher><subject>Animals ; Antioxidants - pharmacology ; Apoptosis - drug effects ; Biological and medical sciences ; body weight ; brain ; Brain - drug effects ; Brain - metabolism ; cAMP-dependent protein kinase ; Food industries ; Fundamental and applied biological sciences. Psychology ; lead ; Lead - toxicity ; lead acetate ; Male ; medicinal properties ; Mice ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; neurotoxicity ; nitric oxide ; oxidative stress ; Oxidative Stress - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; quercetin ; Quercetin - pharmacology ; Reactive Oxygen Species - metabolism ; Signal Transduction - drug effects ; Western blotting</subject><ispartof>Journal of agricultural and food chemistry, 2013-08, Vol.61 (31), p.7630-7635</ispartof><rights>Copyright © 2013 American Chemical Society</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a369t-91bcf6e1d5bf6ae78e0a209235f17fb2a93869acef3f27019955b40f4e0a83b23</citedby><cites>FETCH-LOGICAL-a369t-91bcf6e1d5bf6ae78e0a209235f17fb2a93869acef3f27019955b40f4e0a83b23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://pubs.acs.org/doi/pdf/10.1021/jf303387d$$EPDF$$P50$$Gacs$$H</linktopdf><linktohtml>$$Uhttps://pubs.acs.org/doi/10.1021/jf303387d$$EHTML$$P50$$Gacs$$H</linktohtml><link.rule.ids>314,776,780,2752,27053,27901,27902,56713,56763</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27626833$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23855546$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Chan-Min</creatorcontrib><creatorcontrib>Zheng, Gui-Hong</creatorcontrib><creatorcontrib>Cheng, Chao</creatorcontrib><creatorcontrib>Sun, Jian-Mei</creatorcontrib><title>Quercetin Protects Mouse Brain against Lead-Induced Neurotoxicity</title><title>Journal of agricultural and food chemistry</title><addtitle>J. Agric. Food Chem</addtitle><description>Quercetin (QE), the major bioflavonoid in the human diet, has been reported to have many benefits and medicinal properties. However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxicity in mice exposed to Pb. Mice were exposed to lead acetate (20 mg/kg body weight/day) intragastrically with or without QE (15 and 30 mg/kg body weight/day) coadministration for 3 months. The data showed that QE significantly prevented Pb-induced neurotoxicity in a dose-dependent manner. Exploration of the underlying mechanisms of QE action revealed that QE administration decreased Pb contents in blood (13.2, 19.1%) and brain (17.1, 20.0%). QE markedly increased NO production (39.1, 61.1%) and PKA activity (51.0, 57.8%) in brains of Pb-treated mice. Additionally, QE remarkably suppressed Pb-induced oxidative stress in mouse brain. Western blot analysis showed that QE increased the phosphorylations of Akt, CaMKII nNOS, eNOS, and CREB in brains of Pb-treated mice. The results suggest that QE can inhibit Pb-induced neurotoxicity and partly restore PKA, Akt, NOS, CaMKII, and CREB activities.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>body weight</subject><subject>brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>cAMP-dependent protein kinase</subject><subject>Food industries</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>lead</subject><subject>Lead - toxicity</subject><subject>lead acetate</subject><subject>Male</subject><subject>medicinal properties</subject><subject>Mice</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>neurotoxicity</subject><subject>nitric oxide</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>quercetin</subject><subject>Quercetin - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Western blotting</subject><issn>0021-8561</issn><issn>1520-5118</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0D1PwzAQBmALgWgpDPwByMLAEDjbseOMbcVHpfIl6BxdHLtK1SaVnUj032PU0i4sPsn36HT3EnJJ4Y4Co_cLy4FzlZZHpE8Fg1hQqo5JH0IzVkLSHjnzfgEASqRwSnqMKyFEIvtk-NEZp01b1dG7a1qjWx-9NJ030chh-MR5eH0bTQ2W8aQuO23K6NV0wTbfla7azTk5sbj05mJXB2T2-PA1fo6nb0-T8XAaI5dZG2e00FYaWorCSjSpMoAMMsaFpaktGGZcyQy1sdyyFGiWCVEkYJPgFC8YH5Db7VztGu-dsfnaVSt0m5xC_htDvo8h2KutXXfFypR7-Xd3ADc7gF7j0jqsdeUPLpVMKs6Du946i02OcxfM7JMBTQAop6nih0mofb5oOleHEP5Z6QerGXmJ</recordid><startdate>20130807</startdate><enddate>20130807</enddate><creator>Liu, Chan-Min</creator><creator>Zheng, Gui-Hong</creator><creator>Cheng, Chao</creator><creator>Sun, Jian-Mei</creator><general>American Chemical Society</general><scope>FBQ</scope><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></search><sort><creationdate>20130807</creationdate><title>Quercetin Protects Mouse Brain against Lead-Induced Neurotoxicity</title><author>Liu, Chan-Min ; Zheng, Gui-Hong ; Cheng, Chao ; Sun, Jian-Mei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a369t-91bcf6e1d5bf6ae78e0a209235f17fb2a93869acef3f27019955b40f4e0a83b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>body weight</topic><topic>brain</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>cAMP-dependent protein kinase</topic><topic>Food industries</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>lead</topic><topic>Lead - toxicity</topic><topic>lead acetate</topic><topic>Male</topic><topic>medicinal properties</topic><topic>Mice</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>neurotoxicity</topic><topic>nitric oxide</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>quercetin</topic><topic>Quercetin - pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Chan-Min</creatorcontrib><creatorcontrib>Zheng, Gui-Hong</creatorcontrib><creatorcontrib>Cheng, Chao</creatorcontrib><creatorcontrib>Sun, Jian-Mei</creatorcontrib><collection>AGRIS</collection><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><jtitle>Journal of agricultural and food chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Chan-Min</au><au>Zheng, Gui-Hong</au><au>Cheng, Chao</au><au>Sun, Jian-Mei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quercetin Protects Mouse Brain against Lead-Induced Neurotoxicity</atitle><jtitle>Journal of agricultural and food chemistry</jtitle><addtitle>J. Agric. Food Chem</addtitle><date>2013-08-07</date><risdate>2013</risdate><volume>61</volume><issue>31</issue><spage>7630</spage><epage>7635</epage><pages>7630-7635</pages><issn>0021-8561</issn><eissn>1520-5118</eissn><coden>JAFCAU</coden><abstract>Quercetin (QE), the major bioflavonoid in the human diet, has been reported to have many benefits and medicinal properties. However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxicity in mice exposed to Pb. Mice were exposed to lead acetate (20 mg/kg body weight/day) intragastrically with or without QE (15 and 30 mg/kg body weight/day) coadministration for 3 months. The data showed that QE significantly prevented Pb-induced neurotoxicity in a dose-dependent manner. Exploration of the underlying mechanisms of QE action revealed that QE administration decreased Pb contents in blood (13.2, 19.1%) and brain (17.1, 20.0%). QE markedly increased NO production (39.1, 61.1%) and PKA activity (51.0, 57.8%) in brains of Pb-treated mice. Additionally, QE remarkably suppressed Pb-induced oxidative stress in mouse brain. Western blot analysis showed that QE increased the phosphorylations of Akt, CaMKII nNOS, eNOS, and CREB in brains of Pb-treated mice. The results suggest that QE can inhibit Pb-induced neurotoxicity and partly restore PKA, Akt, NOS, CaMKII, and CREB activities.</abstract><cop>Washington, DC</cop><pub>American Chemical Society</pub><pmid>23855546</pmid><doi>10.1021/jf303387d</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Antioxidants - pharmacology Apoptosis - drug effects Biological and medical sciences body weight brain Brain - drug effects Brain - metabolism cAMP-dependent protein kinase Food industries Fundamental and applied biological sciences. Psychology lead Lead - toxicity lead acetate Male medicinal properties Mice Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology neurotoxicity nitric oxide oxidative stress Oxidative Stress - drug effects Proto-Oncogene Proteins c-akt - metabolism quercetin Quercetin - pharmacology Reactive Oxygen Species - metabolism Signal Transduction - drug effects Western blotting |
| title | Quercetin Protects Mouse Brain against Lead-Induced Neurotoxicity |
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