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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Veröffentlicht in:Molecular biology reports 2023, Vol.50 (1), p.433-442
Hauptverfasser: Varışlı, Behçet, Caglayan, Cuneyt, Kandemir, Fatih Mehmet, Gür, Cihan, Ayna, Adnan, Genç, Aydın, Taysı, Seyithan
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container_issue 1
container_start_page 433
container_title Molecular biology reports
container_volume 50
creator Varışlı, Behçet
Caglayan, Cuneyt
Kandemir, Fatih Mehmet
Gür, Cihan
Ayna, Adnan
Genç, Aydın
Taysı, Seyithan
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
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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. 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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. 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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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