Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats
Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to...
Gespeichert in:
| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2023-11, Vol.37 (11), p.e23471-e23471 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e23471 |
|---|---|
| container_issue | 11 |
| container_start_page | e23471 |
| container_title | Journal of biochemical and molecular toxicology |
| container_volume | 37 |
| creator | Ceylan, Tayfun Akin, Ali Tuğrul Karabulut, Derya Tan, Fazile Cantürk Taşkiran, Mehmet Yakan, Birkan |
| description | Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure. |
| doi_str_mv | 10.1002/jbt.23471 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2839742232</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2887516325</sourcerecordid><originalsourceid>FETCH-LOGICAL-c348t-a6928a675ecd33683aedff55dc40809aff7843a4e241e395c8b58912d5ae587d3</originalsourceid><addsrcrecordid>eNpd0MtKxTAQBuAgiveFLyABN7qo5p50KeINBDfHhauSphNPD21TkxY8b288XhauZmA-foYfoRNKLikh7GpVT5eMC0230D4lZVkQoej2ZpeFUprsoYOUVoQQWWq5i_a4FkpRZvbR62IJ0Y4wT63D4D24CQePp-W6D-9zO4QBcBhwHW074Mb29g2ws3OCBtdrnM_rblzCEDoMH2NIcwScYbRTOkI73nYJjn_mIXq5u13cPBRPz_ePN9dPhePCTIVVJTNWaQmu4VwZbqHxXsrGCWJIab3XRnArgAkKvJTO1NKUlDXSgjS64Yfo_Dt3jPljSFPVt8lB19kBwpwqZnipBWOcZXr2j67CHIf8XVZGS6o4k1ldfCsXQ0oRfDXGtrdxXVFSffVd5b6rTd_Znv4kznUPzZ_8LZh_ArxWeyM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2887516325</pqid></control><display><type>article</type><title>Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats</title><source>Access via Wiley Online Library</source><creator>Ceylan, Tayfun ; Akin, Ali Tuğrul ; Karabulut, Derya ; Tan, Fazile Cantürk ; Taşkiran, Mehmet ; Yakan, Birkan</creator><creatorcontrib>Ceylan, Tayfun ; Akin, Ali Tuğrul ; Karabulut, Derya ; Tan, Fazile Cantürk ; Taşkiran, Mehmet ; Yakan, Birkan</creatorcontrib><description>Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.23471</identifier><identifier>PMID: 37466128</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Apoptosis ; Bioassays ; Brain damage ; Brain injury ; Catalase ; Cerebral cortex ; Cognitive ability ; Comet assay ; Comet nuclei ; Damage detection ; Degeneration ; Deoxyribonucleic acid ; DNA ; DNA damage ; Enzymatic activity ; Free radicals ; Glial fibrillary acidic protein ; Gliosis ; Growth factors ; Impairment ; Inflammation ; Nerve growth factor ; Neurodegeneration ; Neuronal-glial interactions ; Neuroprotection ; Neurotoxicity ; Nonylphenol ; Object recognition ; Oils & fats ; Pattern recognition ; Proteins ; Superoxide dismutase</subject><ispartof>Journal of biochemical and molecular toxicology, 2023-11, Vol.37 (11), p.e23471-e23471</ispartof><rights>2023 The Authors. Journal of Biochemical and Molecular Toxicology published by Wiley Periodicals LLC.</rights><rights>2023. This article is published under http://creativecommons.org/licenses/by-nc/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-c348t-a6928a675ecd33683aedff55dc40809aff7843a4e241e395c8b58912d5ae587d3</citedby><cites>FETCH-LOGICAL-c348t-a6928a675ecd33683aedff55dc40809aff7843a4e241e395c8b58912d5ae587d3</cites><orcidid>0000-0002-1408-8571 ; 0000-0003-0061-6908 ; 0000-0002-0917-0378 ; 0000-0003-2067-6174 ; 0000-0002-0747-2209 ; 0000-0002-5456-4579</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37466128$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ceylan, Tayfun</creatorcontrib><creatorcontrib>Akin, Ali Tuğrul</creatorcontrib><creatorcontrib>Karabulut, Derya</creatorcontrib><creatorcontrib>Tan, Fazile Cantürk</creatorcontrib><creatorcontrib>Taşkiran, Mehmet</creatorcontrib><creatorcontrib>Yakan, Birkan</creatorcontrib><title>Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.</description><subject>Apoptosis</subject><subject>Bioassays</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Catalase</subject><subject>Cerebral cortex</subject><subject>Cognitive ability</subject><subject>Comet assay</subject><subject>Comet nuclei</subject><subject>Damage detection</subject><subject>Degeneration</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Enzymatic activity</subject><subject>Free radicals</subject><subject>Glial fibrillary acidic protein</subject><subject>Gliosis</subject><subject>Growth factors</subject><subject>Impairment</subject><subject>Inflammation</subject><subject>Nerve growth factor</subject><subject>Neurodegeneration</subject><subject>Neuronal-glial interactions</subject><subject>Neuroprotection</subject><subject>Neurotoxicity</subject><subject>Nonylphenol</subject><subject>Object recognition</subject><subject>Oils & fats</subject><subject>Pattern recognition</subject><subject>Proteins</subject><subject>Superoxide dismutase</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpd0MtKxTAQBuAgiveFLyABN7qo5p50KeINBDfHhauSphNPD21TkxY8b288XhauZmA-foYfoRNKLikh7GpVT5eMC0230D4lZVkQoej2ZpeFUprsoYOUVoQQWWq5i_a4FkpRZvbR62IJ0Y4wT63D4D24CQePp-W6D-9zO4QBcBhwHW074Mb29g2ws3OCBtdrnM_rblzCEDoMH2NIcwScYbRTOkI73nYJjn_mIXq5u13cPBRPz_ePN9dPhePCTIVVJTNWaQmu4VwZbqHxXsrGCWJIab3XRnArgAkKvJTO1NKUlDXSgjS64Yfo_Dt3jPljSFPVt8lB19kBwpwqZnipBWOcZXr2j67CHIf8XVZGS6o4k1ldfCsXQ0oRfDXGtrdxXVFSffVd5b6rTd_Znv4kznUPzZ_8LZh_ArxWeyM</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Ceylan, Tayfun</creator><creator>Akin, Ali Tuğrul</creator><creator>Karabulut, Derya</creator><creator>Tan, Fazile Cantürk</creator><creator>Taşkiran, Mehmet</creator><creator>Yakan, Birkan</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1408-8571</orcidid><orcidid>https://orcid.org/0000-0003-0061-6908</orcidid><orcidid>https://orcid.org/0000-0002-0917-0378</orcidid><orcidid>https://orcid.org/0000-0003-2067-6174</orcidid><orcidid>https://orcid.org/0000-0002-0747-2209</orcidid><orcidid>https://orcid.org/0000-0002-5456-4579</orcidid></search><sort><creationdate>20231101</creationdate><title>Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats</title><author>Ceylan, Tayfun ; Akin, Ali Tuğrul ; Karabulut, Derya ; Tan, Fazile Cantürk ; Taşkiran, Mehmet ; Yakan, Birkan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-a6928a675ecd33683aedff55dc40809aff7843a4e241e395c8b58912d5ae587d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Bioassays</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Catalase</topic><topic>Cerebral cortex</topic><topic>Cognitive ability</topic><topic>Comet assay</topic><topic>Comet nuclei</topic><topic>Damage detection</topic><topic>Degeneration</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>Enzymatic activity</topic><topic>Free radicals</topic><topic>Glial fibrillary acidic protein</topic><topic>Gliosis</topic><topic>Growth factors</topic><topic>Impairment</topic><topic>Inflammation</topic><topic>Nerve growth factor</topic><topic>Neurodegeneration</topic><topic>Neuronal-glial interactions</topic><topic>Neuroprotection</topic><topic>Neurotoxicity</topic><topic>Nonylphenol</topic><topic>Object recognition</topic><topic>Oils & fats</topic><topic>Pattern recognition</topic><topic>Proteins</topic><topic>Superoxide dismutase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ceylan, Tayfun</creatorcontrib><creatorcontrib>Akin, Ali Tuğrul</creatorcontrib><creatorcontrib>Karabulut, Derya</creatorcontrib><creatorcontrib>Tan, Fazile Cantürk</creatorcontrib><creatorcontrib>Taşkiran, Mehmet</creatorcontrib><creatorcontrib>Yakan, Birkan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ceylan, Tayfun</au><au>Akin, Ali Tuğrul</au><au>Karabulut, Derya</au><au>Tan, Fazile Cantürk</au><au>Taşkiran, Mehmet</au><au>Yakan, Birkan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2023-11-01</date><risdate>2023</risdate><volume>37</volume><issue>11</issue><spage>e23471</spage><epage>e23471</epage><pages>e23471-e23471</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37466128</pmid><doi>10.1002/jbt.23471</doi><orcidid>https://orcid.org/0000-0002-1408-8571</orcidid><orcidid>https://orcid.org/0000-0003-0061-6908</orcidid><orcidid>https://orcid.org/0000-0002-0917-0378</orcidid><orcidid>https://orcid.org/0000-0003-2067-6174</orcidid><orcidid>https://orcid.org/0000-0002-0747-2209</orcidid><orcidid>https://orcid.org/0000-0002-5456-4579</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1095-6670 |
| ispartof | Journal of biochemical and molecular toxicology, 2023-11, Vol.37 (11), p.e23471-e23471 |
| issn | 1095-6670 1099-0461 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2839742232 |
| source | Access via Wiley Online Library |
| subjects | Apoptosis Bioassays Brain damage Brain injury Catalase Cerebral cortex Cognitive ability Comet assay Comet nuclei Damage detection Degeneration Deoxyribonucleic acid DNA DNA damage Enzymatic activity Free radicals Glial fibrillary acidic protein Gliosis Growth factors Impairment Inflammation Nerve growth factor Neurodegeneration Neuronal-glial interactions Neuroprotection Neurotoxicity Nonylphenol Object recognition Oils & fats Pattern recognition Proteins Superoxide dismutase |
| title | Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T19%3A06%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Therapeutic%20effect%20of%20thymoquinone%20on%20brain%20damage%20caused%20by%20nonylphenol%20exposure%20in%20rats&rft.jtitle=Journal%20of%20biochemical%20and%20molecular%20toxicology&rft.au=Ceylan,%20Tayfun&rft.date=2023-11-01&rft.volume=37&rft.issue=11&rft.spage=e23471&rft.epage=e23471&rft.pages=e23471-e23471&rft.issn=1095-6670&rft.eissn=1099-0461&rft_id=info:doi/10.1002/jbt.23471&rft_dat=%3Cproquest_cross%3E2887516325%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2887516325&rft_id=info:pmid/37466128&rfr_iscdi=true |