Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats
Background Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of...
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description | Background
Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress.
Methods
The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days.
Results
DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of
HO-1
and
Nrf2
in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating
caspase-3, Bax
,
LC3A
, and
LC3B
levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of
ATF-6, IRE1
,
PERK
, and
GRP78
. Additionally, it was observed that DF administration up-regulated
MMP2
and
MMP9
. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue.
Conclusion
Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration. |
doi_str_mv | 10.1007/s11033-022-07928-7 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2849891153</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2849891153</sourcerecordid><originalsourceid>FETCH-LOGICAL-c408t-339d877f3ec44107fc04f9e316b502eaee8efca947cd1c4af7f53b1b31294dcb3</originalsourceid><addsrcrecordid>eNp9kc2KFDEURoMoTs_oC7iQgBsXlt5UUpOqpTTqCANudB1Sya3uDFVJmR-xHsM3NmO3Ci5c5ZKc78uFQ8gzBq8ZgHyTGAPOG2jbBuTQ9o18QHask7wRg-wfkh1wYI3oO3ZBLlO6AwDBZPeYXPBrLkQPfEd-7I9xS87TxWV30BkTtc7MYUKvTeO8LQYtPeKqc8jhuzMub3Tc6BJsmXV2_kDrra3TN6QpR0zpFdVrWHNI7n4sOaxHfdio9pait2GddVqcoRGzM2UuyzlG6xJR5_SEPJr0nPDp-bwiX96_-7y_aW4_ffi4f3vbGAF9bjgfbC_lxNEIwUBOBsQ0IGfXYwctasQeJ6MHIY1lRuhJTh0f2chZOwhrRn5FXp561xi-FkxZLS4ZnGftMZSk2l4M_cBYxyv64h_0LpTo63aqlRK4bBmHSrUnysSQUsRJrdEtOm6KgboXpk7CVBWmfglTsoaen6vLuKD9E_ltqAL8BKT65A8Y__79n9qf6a6lHA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2770372130</pqid></control><display><type>article</type><title>Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Varışlı, Behçet ; Caglayan, Cuneyt ; Kandemir, Fatih Mehmet ; Gür, Cihan ; Ayna, Adnan ; Genç, Aydın ; Taysı, Seyithan</creator><creatorcontrib>Varışlı, Behçet ; Caglayan, Cuneyt ; Kandemir, Fatih Mehmet ; Gür, Cihan ; Ayna, Adnan ; Genç, Aydın ; Taysı, Seyithan</creatorcontrib><description>Background
Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress.
Methods
The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days.
Results
DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of
HO-1
and
Nrf2
in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating
caspase-3, Bax
,
LC3A
, and
LC3B
levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of
ATF-6, IRE1
,
PERK
, and
GRP78
. Additionally, it was observed that DF administration up-regulated
MMP2
and
MMP9
. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue.
Conclusion
Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-022-07928-7</identifier><identifier>PMID: 36344803</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Animals ; Apoptosis ; Autophagy ; Bcl-2 protein ; Biomedical and Life Sciences ; Caspase-3 ; Catalase ; Chemical and Drug Induced Liver Injury - drug therapy ; chrysin ; Diclofenac ; Diclofenac - toxicity ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress ; Gelatinase A ; Gelatinase B ; Glutathione peroxidase ; Hepatotoxicity ; Histology ; Inflammation ; Life Sciences ; Liver ; Morphology ; nonsteroidal anti-inflammatory agents ; Nonsteroidal anti-inflammatory drugs ; Original Article ; Oxidative Stress ; pain ; Rats ; RNA, Messenger ; superoxide dismutase</subject><ispartof>Molecular biology reports, 2023, Vol.50 (1), p.433-442</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-339d877f3ec44107fc04f9e316b502eaee8efca947cd1c4af7f53b1b31294dcb3</citedby><cites>FETCH-LOGICAL-c408t-339d877f3ec44107fc04f9e316b502eaee8efca947cd1c4af7f53b1b31294dcb3</cites><orcidid>0000-0001-5608-554X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-022-07928-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-022-07928-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27913,27914,41477,42546,51308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36344803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Varışlı, Behçet</creatorcontrib><creatorcontrib>Caglayan, Cuneyt</creatorcontrib><creatorcontrib>Kandemir, Fatih Mehmet</creatorcontrib><creatorcontrib>Gür, Cihan</creatorcontrib><creatorcontrib>Ayna, Adnan</creatorcontrib><creatorcontrib>Genç, Aydın</creatorcontrib><creatorcontrib>Taysı, Seyithan</creatorcontrib><title>Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Background
Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress.
Methods
The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days.
Results
DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of
HO-1
and
Nrf2
in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating
caspase-3, Bax
,
LC3A
, and
LC3B
levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of
ATF-6, IRE1
,
PERK
, and
GRP78
. Additionally, it was observed that DF administration up-regulated
MMP2
and
MMP9
. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue.
Conclusion
Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Caspase-3</subject><subject>Catalase</subject><subject>Chemical and Drug Induced Liver Injury - drug therapy</subject><subject>chrysin</subject><subject>Diclofenac</subject><subject>Diclofenac - toxicity</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>Glutathione peroxidase</subject><subject>Hepatotoxicity</subject><subject>Histology</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Morphology</subject><subject>nonsteroidal anti-inflammatory agents</subject><subject>Nonsteroidal anti-inflammatory drugs</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>pain</subject><subject>Rats</subject><subject>RNA, Messenger</subject><subject>superoxide dismutase</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc2KFDEURoMoTs_oC7iQgBsXlt5UUpOqpTTqCANudB1Sya3uDFVJmR-xHsM3NmO3Ci5c5ZKc78uFQ8gzBq8ZgHyTGAPOG2jbBuTQ9o18QHask7wRg-wfkh1wYI3oO3ZBLlO6AwDBZPeYXPBrLkQPfEd-7I9xS87TxWV30BkTtc7MYUKvTeO8LQYtPeKqc8jhuzMub3Tc6BJsmXV2_kDrra3TN6QpR0zpFdVrWHNI7n4sOaxHfdio9pait2GddVqcoRGzM2UuyzlG6xJR5_SEPJr0nPDp-bwiX96_-7y_aW4_ffi4f3vbGAF9bjgfbC_lxNEIwUBOBsQ0IGfXYwctasQeJ6MHIY1lRuhJTh0f2chZOwhrRn5FXp561xi-FkxZLS4ZnGftMZSk2l4M_cBYxyv64h_0LpTo63aqlRK4bBmHSrUnysSQUsRJrdEtOm6KgboXpk7CVBWmfglTsoaen6vLuKD9E_ltqAL8BKT65A8Y__79n9qf6a6lHA</recordid><startdate>2023</startdate><enddate>2023</enddate><creator>Varışlı, Behçet</creator><creator>Caglayan, Cuneyt</creator><creator>Kandemir, Fatih Mehmet</creator><creator>Gür, Cihan</creator><creator>Ayna, Adnan</creator><creator>Genç, Aydın</creator><creator>Taysı, Seyithan</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0001-5608-554X</orcidid></search><sort><creationdate>2023</creationdate><title>Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats</title><author>Varışlı, Behçet ; Caglayan, Cuneyt ; Kandemir, Fatih Mehmet ; Gür, Cihan ; Ayna, Adnan ; Genç, Aydın ; Taysı, Seyithan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-339d877f3ec44107fc04f9e316b502eaee8efca947cd1c4af7f53b1b31294dcb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Caspase-3</topic><topic>Catalase</topic><topic>Chemical and Drug Induced Liver Injury - drug therapy</topic><topic>chrysin</topic><topic>Diclofenac</topic><topic>Diclofenac - toxicity</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress</topic><topic>Gelatinase A</topic><topic>Gelatinase B</topic><topic>Glutathione peroxidase</topic><topic>Hepatotoxicity</topic><topic>Histology</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Morphology</topic><topic>nonsteroidal anti-inflammatory agents</topic><topic>Nonsteroidal anti-inflammatory drugs</topic><topic>Original Article</topic><topic>Oxidative Stress</topic><topic>pain</topic><topic>Rats</topic><topic>RNA, Messenger</topic><topic>superoxide dismutase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Varışlı, Behçet</creatorcontrib><creatorcontrib>Caglayan, Cuneyt</creatorcontrib><creatorcontrib>Kandemir, Fatih Mehmet</creatorcontrib><creatorcontrib>Gür, Cihan</creatorcontrib><creatorcontrib>Ayna, Adnan</creatorcontrib><creatorcontrib>Genç, Aydın</creatorcontrib><creatorcontrib>Taysı, Seyithan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>Engineering Research Database</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>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Varışlı, Behçet</au><au>Caglayan, Cuneyt</au><au>Kandemir, Fatih Mehmet</au><au>Gür, Cihan</au><au>Ayna, Adnan</au><au>Genç, Aydın</au><au>Taysı, Seyithan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2023</date><risdate>2023</risdate><volume>50</volume><issue>1</issue><spage>433</spage><epage>442</epage><pages>433-442</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Background
Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress.
Methods
The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days.
Results
DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of
HO-1
and
Nrf2
in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating
caspase-3, Bax
,
LC3A
, and
LC3B
levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of
ATF-6, IRE1
,
PERK
, and
GRP78
. Additionally, it was observed that DF administration up-regulated
MMP2
and
MMP9
. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue.
Conclusion
Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>36344803</pmid><doi>10.1007/s11033-022-07928-7</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5608-554X</orcidid></addata></record> |
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subjects | Animal Anatomy Animal Biochemistry Animals Apoptosis Autophagy Bcl-2 protein Biomedical and Life Sciences Caspase-3 Catalase Chemical and Drug Induced Liver Injury - drug therapy chrysin Diclofenac Diclofenac - toxicity Endoplasmic reticulum Endoplasmic Reticulum Stress Gelatinase A Gelatinase B Glutathione peroxidase Hepatotoxicity Histology Inflammation Life Sciences Liver Morphology nonsteroidal anti-inflammatory agents Nonsteroidal anti-inflammatory drugs Original Article Oxidative Stress pain Rats RNA, Messenger superoxide dismutase |
title | Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats |
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