Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux
Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredic...
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| Veröffentlicht in: | PloS one 2014-11, Vol.9 (11), p.e112683 |
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| creator | Gu, Hong-Feng Nie, Ya-Xiong Tong, Qiao-Zhen Tang, Ya-Ling Zeng, Yang Jing, Kai-Quan Zheng, Xi-Long Liao, Duan-Fang |
| description | Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1-42 (Aβ1-42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux. |
| doi_str_mv | 10.1371/journal.pone.0112683 |
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Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1-42 (Aβ1-42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0112683</identifier><identifier>PMID: 25393306</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Alzheimer's disease ; Amyloid beta-Peptides - genetics ; Amyloid beta-Peptides - metabolism ; Animal cognition ; Animals ; Apoptosis ; Attenuation ; Autoantigens - genetics ; Autoantigens - metabolism ; Autophagy ; Autophagy - drug effects ; Biochemistry ; Biology and Life Sciences ; Brain research ; CA1 Region, Hippocampal - drug effects ; CA1 Region, Hippocampal - metabolism ; CA1 Region, Hippocampal - pathology ; Catechin - analogs & derivatives ; Catechin - antagonists & inhibitors ; Catechin - pharmacology ; Cell cycle ; Cell death ; Chloroquine ; Chloroquine - pharmacology ; Chronic Disease ; Cognitive ability ; Cognitive Dysfunction - drug therapy ; Cognitive Dysfunction - etiology ; Cognitive Dysfunction - genetics ; Cognitive Dysfunction - physiopathology ; Epigallocatechin gallate ; Fluctuations ; Flux ; Gene Expression Regulation ; Green tea ; Hippocampus ; Hospitals ; Impairment ; Kinases ; Laboratories ; Learning ; Lipids ; Male ; Maze Learning - drug effects ; Medical research ; Medicine ; Medicine and Health Sciences ; Memory ; Memory - drug effects ; Microtubule-Associated Proteins - genetics ; Microtubule-Associated Proteins - metabolism ; Molecular biology ; Neurodegeneration ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Neurosciences ; Nootropic Agents - antagonists & inhibitors ; Nootropic Agents - pharmacology ; p62 Protein ; Peptide Fragments - genetics ; Peptide Fragments - metabolism ; Phagocytosis ; Physiology ; Proteins ; Rapamycin ; Rats ; Rats, Wistar ; Ribosomal protein S6 ; Ribosomal protein S6 kinase ; Ribosomal Protein S6 Kinases, 70-kDa - genetics ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; Rodents ; Signal Transduction ; Signaling ; Stem cells ; Stress ; Stress, Psychological - complications ; Stress, Psychological - drug therapy ; Stress, Psychological - genetics ; Stress, Psychological - physiopathology ; Studies ; Tea ; TOR protein ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>PloS one, 2014-11, Vol.9 (11), p.e112683</ispartof><rights>2014 Gu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (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>2014 Gu et al 2014 Gu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-e78031319d0cc7906221141e84225b883e2a515266d77ac3afb9ceff22cb715a3</citedby><cites>FETCH-LOGICAL-c592t-e78031319d0cc7906221141e84225b883e2a515266d77ac3afb9ceff22cb715a3</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/PMC4231069/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231069/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25393306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, Hong-Feng</creatorcontrib><creatorcontrib>Nie, Ya-Xiong</creatorcontrib><creatorcontrib>Tong, Qiao-Zhen</creatorcontrib><creatorcontrib>Tang, Ya-Ling</creatorcontrib><creatorcontrib>Zeng, Yang</creatorcontrib><creatorcontrib>Jing, Kai-Quan</creatorcontrib><creatorcontrib>Zheng, Xi-Long</creatorcontrib><creatorcontrib>Liao, Duan-Fang</creatorcontrib><title>Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1-42 (Aβ1-42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux.</description><subject>Abnormalities</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - genetics</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animal cognition</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Attenuation</subject><subject>Autoantigens - genetics</subject><subject>Autoantigens - metabolism</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Brain research</subject><subject>CA1 Region, Hippocampal - drug effects</subject><subject>CA1 Region, Hippocampal - metabolism</subject><subject>CA1 Region, Hippocampal - pathology</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - antagonists & inhibitors</subject><subject>Catechin - pharmacology</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Chloroquine</subject><subject>Chloroquine - pharmacology</subject><subject>Chronic Disease</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction - drug therapy</subject><subject>Cognitive Dysfunction - etiology</subject><subject>Cognitive Dysfunction - genetics</subject><subject>Cognitive Dysfunction - physiopathology</subject><subject>Epigallocatechin gallate</subject><subject>Fluctuations</subject><subject>Flux</subject><subject>Gene Expression Regulation</subject><subject>Green tea</subject><subject>Hippocampus</subject><subject>Hospitals</subject><subject>Impairment</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Learning</subject><subject>Lipids</subject><subject>Male</subject><subject>Maze Learning - drug effects</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Memory</subject><subject>Memory - drug effects</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Molecular biology</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurosciences</subject><subject>Nootropic Agents - antagonists & inhibitors</subject><subject>Nootropic Agents - pharmacology</subject><subject>p62 Protein</subject><subject>Peptide Fragments - genetics</subject><subject>Peptide Fragments - metabolism</subject><subject>Phagocytosis</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ribosomal protein S6</subject><subject>Ribosomal protein S6 kinase</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - genetics</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Stress</subject><subject>Stress, Psychological - complications</subject><subject>Stress, Psychological - drug therapy</subject><subject>Stress, Psychological - genetics</subject><subject>Stress, Psychological - physiopathology</subject><subject>Studies</subject><subject>Tea</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - genetics</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIlsI_QGCJC5cs_oid-IKEqgKVKnGBs-U4k12vHDvYDmL_Dr8UbzetWsTFnhm_efPhV1WvCd4Q1pIP-7BEr91mDh42mBAqOvakOieS0VpQzJ4-sM-qFyntMeasE-J5dUY5k4xhcV79uZrtVjsXjM5gdtbXrD76xUM6Z_BLsRKy06xtnMBnFEbkQEdv_RZpP6AJphAPyHpkdjF4a9Di5wiDNVn3DtBk3YBSjpBSXc5CN6Coc0L9AZVgDvHItLPzXHooZRzSSw7zTm8L1eiW3y-rZ6N2CV6t90X14_PV98uv9c23L9eXn25qwyXNNbQdZoQROWBjWokFpYQ0BLqGUt53HQOqOeFUiKFttWF67KWBcaTU9C3hml1Ub0-8swtJretNigjayEYyyQvi-oQYgt6rOdpJx4MK2qrbQIhbpWO2xoHqAQwTwHss2qYB1hvSkbExvO1LE50pXB_Xaks_wWDKaqN2j0gfv3i7U9vwSzWUESxkIXi_EsTwcymLVJNNBsrXeQjLbd-cNaSVXYG--wf6_-maE8rEkFKE8b4ZgtVRcndZ6ig5tUqupL15OMh90p3G2F8f8dkV</recordid><startdate>20141113</startdate><enddate>20141113</enddate><creator>Gu, Hong-Feng</creator><creator>Nie, Ya-Xiong</creator><creator>Tong, Qiao-Zhen</creator><creator>Tang, Ya-Ling</creator><creator>Zeng, Yang</creator><creator>Jing, Kai-Quan</creator><creator>Zheng, Xi-Long</creator><creator>Liao, Duan-Fang</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>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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20141113</creationdate><title>Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux</title><author>Gu, Hong-Feng ; Nie, Ya-Xiong ; Tong, Qiao-Zhen ; Tang, Ya-Ling ; Zeng, Yang ; Jing, Kai-Quan ; Zheng, Xi-Long ; Liao, Duan-Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-e78031319d0cc7906221141e84225b883e2a515266d77ac3afb9ceff22cb715a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abnormalities</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - 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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>MEDLINE - Academic</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>Gu, Hong-Feng</au><au>Nie, Ya-Xiong</au><au>Tong, Qiao-Zhen</au><au>Tang, Ya-Ling</au><au>Zeng, Yang</au><au>Jing, Kai-Quan</au><au>Zheng, Xi-Long</au><au>Liao, Duan-Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-11-13</date><risdate>2014</risdate><volume>9</volume><issue>11</issue><spage>e112683</spage><pages>e112683-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1-42 (Aβ1-42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25393306</pmid><doi>10.1371/journal.pone.0112683</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-11, Vol.9 (11), p.e112683 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1624949395 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Abnormalities Alzheimer's disease Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Animal cognition Animals Apoptosis Attenuation Autoantigens - genetics Autoantigens - metabolism Autophagy Autophagy - drug effects Biochemistry Biology and Life Sciences Brain research CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - metabolism CA1 Region, Hippocampal - pathology Catechin - analogs & derivatives Catechin - antagonists & inhibitors Catechin - pharmacology Cell cycle Cell death Chloroquine Chloroquine - pharmacology Chronic Disease Cognitive ability Cognitive Dysfunction - drug therapy Cognitive Dysfunction - etiology Cognitive Dysfunction - genetics Cognitive Dysfunction - physiopathology Epigallocatechin gallate Fluctuations Flux Gene Expression Regulation Green tea Hippocampus Hospitals Impairment Kinases Laboratories Learning Lipids Male Maze Learning - drug effects Medical research Medicine Medicine and Health Sciences Memory Memory - drug effects Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - metabolism Molecular biology Neurodegeneration Neurology Neurons Neurons - drug effects Neurons - metabolism Neurons - pathology Neurosciences Nootropic Agents - antagonists & inhibitors Nootropic Agents - pharmacology p62 Protein Peptide Fragments - genetics Peptide Fragments - metabolism Phagocytosis Physiology Proteins Rapamycin Rats Rats, Wistar Ribosomal protein S6 Ribosomal protein S6 kinase Ribosomal Protein S6 Kinases, 70-kDa - genetics Ribosomal Protein S6 Kinases, 70-kDa - metabolism Rodents Signal Transduction Signaling Stem cells Stress Stress, Psychological - complications Stress, Psychological - drug therapy Stress, Psychological - genetics Stress, Psychological - physiopathology Studies Tea TOR protein TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism |
| title | Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux |
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