Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury
Aims The aim of this study was to evaluate the effect of epicatechin, on neurological recovery and neuroinflammation after traumatic brain injury (TBI) to investigate its potential value in clinical practice. Methods TBI model was established in adult rats by CCI method. The effect of epicatechin wa...
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| Veröffentlicht in: | CNS neuroscience & therapeutics 2024-02, Vol.30 (2), p.e14364-n/a |
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| creator | Wang, Ziheng Lu, Zhichao Chen, Yixun Wang, Chenxing Gong, Peipei Jiang, Rui Liu, Qianqian |
| description | Aims
The aim of this study was to evaluate the effect of epicatechin, on neurological recovery and neuroinflammation after traumatic brain injury (TBI) to investigate its potential value in clinical practice.
Methods
TBI model was established in adult rats by CCI method. The effect of epicatechin was evaluated after intraperitoneal injection. Neurological recovery after TBI was assessed by Morris Water Maze, mNSS score, Rotarod test and Adhesive removal test. Protein and gene expression was assessed by Western blot, ELISA, PCR and immunofluorescence. Furthermore, the use of AKT pathway inhibitors blocked the therapeutic effects of epicatechin clarifying AKT‐P53/CREB as a potential pathway for the effects of epicatechin.
Results
Administering epicatechin after TBI prevented neuronal death, reduced neuroinflammation, and promoted neurological function restoration in TBI rats. Network pharmacology study suggested that epicatechin may exert its therapeutic benefits through the AKT‐P53/CREB pathway
Conclusion
These results indicate that epicatechin, a monomeric compound derived from tea polyphenols, possesses potent antioxidant and anti‐inflammatory properties after TBI. The mechanism may be related to the regulation of the AKT‐P53/CREB signal pathway.
Epicatechin has therapeutic benefits via the AKT‐P53/CREB pathway by network pharmacology study. These results imply that epicatechin is a potentially effective therapy for neurological impairments following TBI. |
| doi_str_mv | 10.1111/cns.14364 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10848092</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A800016303</galeid><sourcerecordid>A800016303</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5114-1185d6c52380d34285b690c93c64c871bb3a4f0eff368ac792a709c4e6e8371c3</originalsourceid><addsrcrecordid>eNp1kdGO1CAUhonRuOvohS9gSLzRi5mBQilcmXGyq8aNGh2vCaW0ZdJChXYnc-cj7DP6JOJ2naiJcHEIfOc_5_AD8BSjFU5rrV1cYUoYvQfOcZHny1xQcf90JugMPIpxjxDLuOAPwRkpKKM5F-eg3qnQmNG6Bo6tgZv3ux_fbz7lZL39fPEaDmpsD-oID3ZsoRmsVqPRrXWw9gHafgj-2lQwhcb5aCP0NRyDmno1Wg3LoBJp3X4Kx8fgQa26aJ7cxQX4enmx275dXn188267uVrqHGO6xJjnFdN5RjiqCM14XjKBtCCaUc0LXJZE0RqZuiaMK12ITBVIaGqY4aTAmizAq1l3mMreVNq41E8nh2B7FY7SKyv_fnG2lY2_lhhxypHIksKLO4Xgv00mjrK3UZuuU874KcqME1FQzG7R5_-gez8Fl-aTmSCEIM7T5y_AaqYa1RlpXe1TYZ12ZXqrvTO1TfcbjhDCjCCSEl7OCTr4GIOpT-1jJH_5LZPf8tbvxD77c94T-dvgBKxn4JCqHP-vJLcfvsySPwF-s7UJ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2933308859</pqid></control><display><type>article</type><title>Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury</title><source>Wiley Journals</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Wang, Ziheng ; Lu, Zhichao ; Chen, Yixun ; Wang, Chenxing ; Gong, Peipei ; Jiang, Rui ; Liu, Qianqian</creator><creatorcontrib>Wang, Ziheng ; Lu, Zhichao ; Chen, Yixun ; Wang, Chenxing ; Gong, Peipei ; Jiang, Rui ; Liu, Qianqian</creatorcontrib><description>Aims
The aim of this study was to evaluate the effect of epicatechin, on neurological recovery and neuroinflammation after traumatic brain injury (TBI) to investigate its potential value in clinical practice.
Methods
TBI model was established in adult rats by CCI method. The effect of epicatechin was evaluated after intraperitoneal injection. Neurological recovery after TBI was assessed by Morris Water Maze, mNSS score, Rotarod test and Adhesive removal test. Protein and gene expression was assessed by Western blot, ELISA, PCR and immunofluorescence. Furthermore, the use of AKT pathway inhibitors blocked the therapeutic effects of epicatechin clarifying AKT‐P53/CREB as a potential pathway for the effects of epicatechin.
Results
Administering epicatechin after TBI prevented neuronal death, reduced neuroinflammation, and promoted neurological function restoration in TBI rats. Network pharmacology study suggested that epicatechin may exert its therapeutic benefits through the AKT‐P53/CREB pathway
Conclusion
These results indicate that epicatechin, a monomeric compound derived from tea polyphenols, possesses potent antioxidant and anti‐inflammatory properties after TBI. The mechanism may be related to the regulation of the AKT‐P53/CREB signal pathway.
Epicatechin has therapeutic benefits via the AKT‐P53/CREB pathway by network pharmacology study. These results imply that epicatechin is a potentially effective therapy for neurological impairments following TBI.</description><identifier>ISSN: 1755-5930</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.14364</identifier><identifier>PMID: 37464589</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adhesives ; AKT protein ; Alzheimer's disease ; Anti-inflammatory agents ; Antibodies ; Antigens ; Biotechnology industry ; Brain ; Chemokines ; Cocoa ; Cyclic AMP response element-binding protein ; Cytokines ; Enzyme-linked immunosorbent assay ; Epicatechin ; Gene expression ; Hydraulics ; Immunofluorescence ; Inflammation ; Injuries ; International economic relations ; Kinases ; microglia ; neurological function ; Neurons ; Original ; p53 Protein ; Polymerase chain reaction ; Polyphenols ; Proteins ; Traumatic brain injury ; Tumor necrosis factor-TNF</subject><ispartof>CNS neuroscience & therapeutics, 2024-02, Vol.30 (2), p.e14364-n/a</ispartof><rights>2023 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.</rights><rights>COPYRIGHT 2024 John Wiley & Sons, Inc.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5114-1185d6c52380d34285b690c93c64c871bb3a4f0eff368ac792a709c4e6e8371c3</citedby><cites>FETCH-LOGICAL-c5114-1185d6c52380d34285b690c93c64c871bb3a4f0eff368ac792a709c4e6e8371c3</cites><orcidid>0000-0001-8873-732X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848092/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848092/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37464589$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Ziheng</creatorcontrib><creatorcontrib>Lu, Zhichao</creatorcontrib><creatorcontrib>Chen, Yixun</creatorcontrib><creatorcontrib>Wang, Chenxing</creatorcontrib><creatorcontrib>Gong, Peipei</creatorcontrib><creatorcontrib>Jiang, Rui</creatorcontrib><creatorcontrib>Liu, Qianqian</creatorcontrib><title>Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury</title><title>CNS neuroscience & therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>Aims
The aim of this study was to evaluate the effect of epicatechin, on neurological recovery and neuroinflammation after traumatic brain injury (TBI) to investigate its potential value in clinical practice.
Methods
TBI model was established in adult rats by CCI method. The effect of epicatechin was evaluated after intraperitoneal injection. Neurological recovery after TBI was assessed by Morris Water Maze, mNSS score, Rotarod test and Adhesive removal test. Protein and gene expression was assessed by Western blot, ELISA, PCR and immunofluorescence. Furthermore, the use of AKT pathway inhibitors blocked the therapeutic effects of epicatechin clarifying AKT‐P53/CREB as a potential pathway for the effects of epicatechin.
Results
Administering epicatechin after TBI prevented neuronal death, reduced neuroinflammation, and promoted neurological function restoration in TBI rats. Network pharmacology study suggested that epicatechin may exert its therapeutic benefits through the AKT‐P53/CREB pathway
Conclusion
These results indicate that epicatechin, a monomeric compound derived from tea polyphenols, possesses potent antioxidant and anti‐inflammatory properties after TBI. The mechanism may be related to the regulation of the AKT‐P53/CREB signal pathway.
Epicatechin has therapeutic benefits via the AKT‐P53/CREB pathway by network pharmacology study. These results imply that epicatechin is a potentially effective therapy for neurological impairments following TBI.</description><subject>Adhesives</subject><subject>AKT protein</subject><subject>Alzheimer's disease</subject><subject>Anti-inflammatory agents</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Biotechnology industry</subject><subject>Brain</subject><subject>Chemokines</subject><subject>Cocoa</subject><subject>Cyclic AMP response element-binding protein</subject><subject>Cytokines</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epicatechin</subject><subject>Gene expression</subject><subject>Hydraulics</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>International economic relations</subject><subject>Kinases</subject><subject>microglia</subject><subject>neurological function</subject><subject>Neurons</subject><subject>Original</subject><subject>p53 Protein</subject><subject>Polymerase chain reaction</subject><subject>Polyphenols</subject><subject>Proteins</subject><subject>Traumatic brain injury</subject><subject>Tumor necrosis factor-TNF</subject><issn>1755-5930</issn><issn>1755-5949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kdGO1CAUhonRuOvohS9gSLzRi5mBQilcmXGyq8aNGh2vCaW0ZdJChXYnc-cj7DP6JOJ2naiJcHEIfOc_5_AD8BSjFU5rrV1cYUoYvQfOcZHny1xQcf90JugMPIpxjxDLuOAPwRkpKKM5F-eg3qnQmNG6Bo6tgZv3ux_fbz7lZL39fPEaDmpsD-oID3ZsoRmsVqPRrXWw9gHafgj-2lQwhcb5aCP0NRyDmno1Wg3LoBJp3X4Kx8fgQa26aJ7cxQX4enmx275dXn188267uVrqHGO6xJjnFdN5RjiqCM14XjKBtCCaUc0LXJZE0RqZuiaMK12ITBVIaGqY4aTAmizAq1l3mMreVNq41E8nh2B7FY7SKyv_fnG2lY2_lhhxypHIksKLO4Xgv00mjrK3UZuuU874KcqME1FQzG7R5_-gez8Fl-aTmSCEIM7T5y_AaqYa1RlpXe1TYZ12ZXqrvTO1TfcbjhDCjCCSEl7OCTr4GIOpT-1jJH_5LZPf8tbvxD77c94T-dvgBKxn4JCqHP-vJLcfvsySPwF-s7UJ</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Wang, Ziheng</creator><creator>Lu, Zhichao</creator><creator>Chen, Yixun</creator><creator>Wang, Chenxing</creator><creator>Gong, Peipei</creator><creator>Jiang, Rui</creator><creator>Liu, Qianqian</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8873-732X</orcidid></search><sort><creationdate>202402</creationdate><title>Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury</title><author>Wang, Ziheng ; Lu, Zhichao ; Chen, Yixun ; Wang, Chenxing ; Gong, Peipei ; Jiang, Rui ; Liu, Qianqian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5114-1185d6c52380d34285b690c93c64c871bb3a4f0eff368ac792a709c4e6e8371c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adhesives</topic><topic>AKT protein</topic><topic>Alzheimer's disease</topic><topic>Anti-inflammatory agents</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Biotechnology industry</topic><topic>Brain</topic><topic>Chemokines</topic><topic>Cocoa</topic><topic>Cyclic AMP response element-binding protein</topic><topic>Cytokines</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epicatechin</topic><topic>Gene expression</topic><topic>Hydraulics</topic><topic>Immunofluorescence</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>International economic relations</topic><topic>Kinases</topic><topic>microglia</topic><topic>neurological function</topic><topic>Neurons</topic><topic>Original</topic><topic>p53 Protein</topic><topic>Polymerase chain reaction</topic><topic>Polyphenols</topic><topic>Proteins</topic><topic>Traumatic brain injury</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Ziheng</creatorcontrib><creatorcontrib>Lu, Zhichao</creatorcontrib><creatorcontrib>Chen, Yixun</creatorcontrib><creatorcontrib>Wang, Chenxing</creatorcontrib><creatorcontrib>Gong, Peipei</creatorcontrib><creatorcontrib>Jiang, Rui</creatorcontrib><creatorcontrib>Liu, Qianqian</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Ziheng</au><au>Lu, Zhichao</au><au>Chen, Yixun</au><au>Wang, Chenxing</au><au>Gong, Peipei</au><au>Jiang, Rui</au><au>Liu, Qianqian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury</atitle><jtitle>CNS neuroscience & therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2024-02</date><risdate>2024</risdate><volume>30</volume><issue>2</issue><spage>e14364</spage><epage>n/a</epage><pages>e14364-n/a</pages><issn>1755-5930</issn><eissn>1755-5949</eissn><abstract>Aims
The aim of this study was to evaluate the effect of epicatechin, on neurological recovery and neuroinflammation after traumatic brain injury (TBI) to investigate its potential value in clinical practice.
Methods
TBI model was established in adult rats by CCI method. The effect of epicatechin was evaluated after intraperitoneal injection. Neurological recovery after TBI was assessed by Morris Water Maze, mNSS score, Rotarod test and Adhesive removal test. Protein and gene expression was assessed by Western blot, ELISA, PCR and immunofluorescence. Furthermore, the use of AKT pathway inhibitors blocked the therapeutic effects of epicatechin clarifying AKT‐P53/CREB as a potential pathway for the effects of epicatechin.
Results
Administering epicatechin after TBI prevented neuronal death, reduced neuroinflammation, and promoted neurological function restoration in TBI rats. Network pharmacology study suggested that epicatechin may exert its therapeutic benefits through the AKT‐P53/CREB pathway
Conclusion
These results indicate that epicatechin, a monomeric compound derived from tea polyphenols, possesses potent antioxidant and anti‐inflammatory properties after TBI. The mechanism may be related to the regulation of the AKT‐P53/CREB signal pathway.
Epicatechin has therapeutic benefits via the AKT‐P53/CREB pathway by network pharmacology study. These results imply that epicatechin is a potentially effective therapy for neurological impairments following TBI.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>37464589</pmid><doi>10.1111/cns.14364</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-8873-732X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Wiley Journals; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Adhesives AKT protein Alzheimer's disease Anti-inflammatory agents Antibodies Antigens Biotechnology industry Brain Chemokines Cocoa Cyclic AMP response element-binding protein Cytokines Enzyme-linked immunosorbent assay Epicatechin Gene expression Hydraulics Immunofluorescence Inflammation Injuries International economic relations Kinases microglia neurological function Neurons Original p53 Protein Polymerase chain reaction Polyphenols Proteins Traumatic brain injury Tumor necrosis factor-TNF |
| title | Targeting the AKT‐P53/CREB pathway with epicatechin for improved prognosis of traumatic brain injury |
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