Possible activation of NRF2 by Vitamin E/Curcumin against altered thyroid hormone induced oxidative stress via NFĸB/AKT/mTOR/KEAP1 signalling in rat heart
Oxidative stress is implicated in both hypo- and hyper-thyroid conditions. In the present study an attempt has been made to elucidate possible interaction between vitamin E or/and curcumin (two established antioxidants) with active portion (redox signaling intervening region) of nuclear factor eryth...
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| Veröffentlicht in: | Scientific reports 2019-05, Vol.9 (1), p.7408, Article 7408 |
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| description | Oxidative stress is implicated in both hypo- and hyper-thyroid conditions. In the present study an attempt has been made to elucidate possible interaction between vitamin E or/and curcumin (two established antioxidants) with active portion (redox signaling intervening region) of nuclear factor erythroid 2-related factor 2 (NRF2) as a mechanism to alleviate oxidative stress in rat heart under altered thyroid states. Fifty Wistar strain rats were divided into two clusters (Cluster A: hypothyroidism; Cluster B: hyperthyroidism). The hypo- (0.05% (w/v) propylthiouracil in drinking water) and hyper- (0.0012% (w/v) T4 in drinking water) thyroid rats in both clusters were supplemented orally with antioxidants (vitamin E or/and curcumin) for 30 days. Interactive least count difference and principal component analyses indicated increase in lipid peroxidation, reduced glutathione level, alteration in the activities and protein expression of antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase under altered thyroid states. However, the expression of stress survival molecules; nuclear factor κB (NFκB) and the serine-threonine kinase B (Akt), in hyper-thyroidism only points towards different mechanisms responsible for either condition. Co-administration of vitamin E and curcumin showed better result in attenuating expression of mammalian target for rapamycin (mTOR), restoration of total protein content and biological activity of Ca
2+
ATPase in hyperthyroid rats, whereas, their individual treatment showed partial restoration. Since NRF2 is responsible for activation of antioxidant response element and subsequent expression of antioxidant enzymes, possible interactions of both vitamin E or/and curcumin with the antioxidant enzymes, NRF2 and its regulator Kelch ECH associating protein (KEAP1) were studied
in silico
. For the first time, a modeled active portion of the zipped protein NRF2 indicated its interaction with both vitamin E and curcumin. Further, curcumin and vitamin E complex showed
in silico
interaction with KEAP1. Reduction of oxidative stress by curcumin and/or vitamin E may be due to modulation of NRF2 and KEAP1 function in rat heart under altered thyroid states. |
| doi_str_mv | 10.1038/s41598-019-43320-5 |
| format | Article |
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2+
ATPase in hyperthyroid rats, whereas, their individual treatment showed partial restoration. Since NRF2 is responsible for activation of antioxidant response element and subsequent expression of antioxidant enzymes, possible interactions of both vitamin E or/and curcumin with the antioxidant enzymes, NRF2 and its regulator Kelch ECH associating protein (KEAP1) were studied
in silico
. For the first time, a modeled active portion of the zipped protein NRF2 indicated its interaction with both vitamin E and curcumin. Further, curcumin and vitamin E complex showed
in silico
interaction with KEAP1. Reduction of oxidative stress by curcumin and/or vitamin E may be due to modulation of NRF2 and KEAP1 function in rat heart under altered thyroid states.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-43320-5</identifier><identifier>PMID: 31092832</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/95 ; 38/77 ; 631/601/1332 ; 64 ; 692/4017 ; 82/1 ; 82/29 ; 82/80 ; 96/95 ; Adenosine triphosphatase ; AKT protein ; Animals ; Antioxidants ; Antioxidants - pharmacology ; Biological activity ; Blotting, Western ; Ca2+-transporting ATPase ; Calcium ; Calcium-Transporting ATPases - metabolism ; Catalase ; Curcumin ; Curcumin - pharmacology ; Drinking water ; Enzymes ; Glutathione peroxidase ; Glutathione reductase ; Heart ; Heart - drug effects ; Humanities and Social Sciences ; Hyperthyroidism ; Hyperthyroidism - metabolism ; Hypothyroidism ; Hypothyroidism - metabolism ; Kelch-Like ECH-Associated Protein 1 - metabolism ; Lipid peroxidation ; Lipid Peroxidation - drug effects ; Male ; multidisciplinary ; Myocardium - metabolism ; NF-E2-Related Factor 2 - metabolism ; NF-kappa B - metabolism ; NF-κB protein ; Oxidative stress ; Oxidative Stress - drug effects ; Peroxidation ; Propylthiouracil ; Protein-serine/threonine kinase ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Rapamycin ; Rats ; Rats, Wistar ; Science ; Science (multidisciplinary) ; Signal Transduction - drug effects ; Superoxide dismutase ; Thyroid ; Thyroid gland ; Thyroid Hormones - metabolism ; Vitamin E ; Vitamin E - pharmacology</subject><ispartof>Scientific reports, 2019-05, Vol.9 (1), p.7408, Article 7408</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. 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-c3895-7a97b0a837f319407097f258cba7b99b00071cc779ef2188f39cde3a6b30e2523</citedby><cites>FETCH-LOGICAL-c3895-7a97b0a837f319407097f258cba7b99b00071cc779ef2188f39cde3a6b30e2523</cites><orcidid>0000-0002-2969-0071 ; 0000-0002-5285-6578</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/PMC6520394/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520394/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,41101,42170,51557,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31092832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mishra, Pallavi</creatorcontrib><creatorcontrib>Paital, Biswaranjan</creatorcontrib><creatorcontrib>Jena, Srikanta</creatorcontrib><creatorcontrib>Swain, Shasank S.</creatorcontrib><creatorcontrib>Kumar, Sunil</creatorcontrib><creatorcontrib>Yadav, Manoj K.</creatorcontrib><creatorcontrib>Chainy, Gagan B. N.</creatorcontrib><creatorcontrib>Samanta, Luna</creatorcontrib><title>Possible activation of NRF2 by Vitamin E/Curcumin against altered thyroid hormone induced oxidative stress via NFĸB/AKT/mTOR/KEAP1 signalling in rat heart</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Oxidative stress is implicated in both hypo- and hyper-thyroid conditions. In the present study an attempt has been made to elucidate possible interaction between vitamin E or/and curcumin (two established antioxidants) with active portion (redox signaling intervening region) of nuclear factor erythroid 2-related factor 2 (NRF2) as a mechanism to alleviate oxidative stress in rat heart under altered thyroid states. Fifty Wistar strain rats were divided into two clusters (Cluster A: hypothyroidism; Cluster B: hyperthyroidism). The hypo- (0.05% (w/v) propylthiouracil in drinking water) and hyper- (0.0012% (w/v) T4 in drinking water) thyroid rats in both clusters were supplemented orally with antioxidants (vitamin E or/and curcumin) for 30 days. Interactive least count difference and principal component analyses indicated increase in lipid peroxidation, reduced glutathione level, alteration in the activities and protein expression of antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase under altered thyroid states. However, the expression of stress survival molecules; nuclear factor κB (NFκB) and the serine-threonine kinase B (Akt), in hyper-thyroidism only points towards different mechanisms responsible for either condition. Co-administration of vitamin E and curcumin showed better result in attenuating expression of mammalian target for rapamycin (mTOR), restoration of total protein content and biological activity of Ca
2+
ATPase in hyperthyroid rats, whereas, their individual treatment showed partial restoration. Since NRF2 is responsible for activation of antioxidant response element and subsequent expression of antioxidant enzymes, possible interactions of both vitamin E or/and curcumin with the antioxidant enzymes, NRF2 and its regulator Kelch ECH associating protein (KEAP1) were studied
in silico
. For the first time, a modeled active portion of the zipped protein NRF2 indicated its interaction with both vitamin E and curcumin. Further, curcumin and vitamin E complex showed
in silico
interaction with KEAP1. Reduction of oxidative stress by curcumin and/or vitamin E may be due to modulation of NRF2 and KEAP1 function in rat heart under altered thyroid states.</description><subject>13/95</subject><subject>38/77</subject><subject>631/601/1332</subject><subject>64</subject><subject>692/4017</subject><subject>82/1</subject><subject>82/29</subject><subject>82/80</subject><subject>96/95</subject><subject>Adenosine triphosphatase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Biological activity</subject><subject>Blotting, Western</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium</subject><subject>Calcium-Transporting ATPases - metabolism</subject><subject>Catalase</subject><subject>Curcumin</subject><subject>Curcumin - pharmacology</subject><subject>Drinking water</subject><subject>Enzymes</subject><subject>Glutathione peroxidase</subject><subject>Glutathione reductase</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Humanities and Social Sciences</subject><subject>Hyperthyroidism</subject><subject>Hyperthyroidism - metabolism</subject><subject>Hypothyroidism</subject><subject>Hypothyroidism - metabolism</subject><subject>Kelch-Like ECH-Associated Protein 1 - metabolism</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>multidisciplinary</subject><subject>Myocardium - metabolism</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidation</subject><subject>Propylthiouracil</subject><subject>Protein-serine/threonine kinase</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rapamycin</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal Transduction - drug effects</subject><subject>Superoxide dismutase</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid Hormones - metabolism</subject><subject>Vitamin E</subject><subject>Vitamin E - pharmacology</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp9UU1u1DAUthAVrdpegAWyxDqNf-I63iANoxlArdqqGthajuNkXCV2sZ0Rc5ZepAfgYHiYUsoGb_zk9_285w-AtxidYUTrMlaYibpAWBQVpQQV7BU4IqhiBaGEvH5RH4LTGO9QPoyICos34JBiJEhNyRF4uPEx2mYwUOlkNypZ76Dv4NXtksBmC7_ZpEbr4KKcT0FPu1L1yrqYoBqSCaaFab0N3rZw7cPonYHWtZPO7_6HbbPexsCYgokRbqyCV8ufjx_L2cWqHFfXt-XFYnaDYbS9U8NgXZ_JMKgE10aFdAIOOjVEc_p0H4Ovy8Vq_rm4vP70ZT67LDStBSu4ErxBqqa8o1hUiCPBO8Jq3SjeCNHkxTnWmnNhOoLruqNCt4aq84YiQxihx-DDXvd-akbTauNSUIO8D3ZUYSu9svLfjrNr2fuNPGcEUVFlgfdPAsF_n0xM8s5PIa8UJSF5Ekw53tmQPUqH_OfBdM8OGMldpnKfqcyZyt-ZSpZJ717O9kz5k2AG0D0g5pbrTfjr_R_ZX9oArjQ</recordid><startdate>20190515</startdate><enddate>20190515</enddate><creator>Mishra, Pallavi</creator><creator>Paital, Biswaranjan</creator><creator>Jena, Srikanta</creator><creator>Swain, Shasank S.</creator><creator>Kumar, Sunil</creator><creator>Yadav, Manoj K.</creator><creator>Chainy, Gagan B. 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N. ; Samanta, Luna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3895-7a97b0a837f319407097f258cba7b99b00071cc779ef2188f39cde3a6b30e2523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/95</topic><topic>38/77</topic><topic>631/601/1332</topic><topic>64</topic><topic>692/4017</topic><topic>82/1</topic><topic>82/29</topic><topic>82/80</topic><topic>96/95</topic><topic>Adenosine triphosphatase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Biological activity</topic><topic>Blotting, Western</topic><topic>Ca2+-transporting ATPase</topic><topic>Calcium</topic><topic>Calcium-Transporting ATPases - metabolism</topic><topic>Catalase</topic><topic>Curcumin</topic><topic>Curcumin - pharmacology</topic><topic>Drinking water</topic><topic>Enzymes</topic><topic>Glutathione peroxidase</topic><topic>Glutathione reductase</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Humanities and Social Sciences</topic><topic>Hyperthyroidism</topic><topic>Hyperthyroidism - metabolism</topic><topic>Hypothyroidism</topic><topic>Hypothyroidism - metabolism</topic><topic>Kelch-Like ECH-Associated Protein 1 - metabolism</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>multidisciplinary</topic><topic>Myocardium - metabolism</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Peroxidation</topic><topic>Propylthiouracil</topic><topic>Protein-serine/threonine kinase</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rapamycin</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Signal Transduction - drug effects</topic><topic>Superoxide dismutase</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid Hormones - metabolism</topic><topic>Vitamin E</topic><topic>Vitamin E - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mishra, Pallavi</creatorcontrib><creatorcontrib>Paital, Biswaranjan</creatorcontrib><creatorcontrib>Jena, Srikanta</creatorcontrib><creatorcontrib>Swain, Shasank S.</creatorcontrib><creatorcontrib>Kumar, Sunil</creatorcontrib><creatorcontrib>Yadav, Manoj K.</creatorcontrib><creatorcontrib>Chainy, Gagan B. 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N.</au><au>Samanta, Luna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible activation of NRF2 by Vitamin E/Curcumin against altered thyroid hormone induced oxidative stress via NFĸB/AKT/mTOR/KEAP1 signalling in rat heart</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-05-15</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>7408</spage><pages>7408-</pages><artnum>7408</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Oxidative stress is implicated in both hypo- and hyper-thyroid conditions. In the present study an attempt has been made to elucidate possible interaction between vitamin E or/and curcumin (two established antioxidants) with active portion (redox signaling intervening region) of nuclear factor erythroid 2-related factor 2 (NRF2) as a mechanism to alleviate oxidative stress in rat heart under altered thyroid states. Fifty Wistar strain rats were divided into two clusters (Cluster A: hypothyroidism; Cluster B: hyperthyroidism). The hypo- (0.05% (w/v) propylthiouracil in drinking water) and hyper- (0.0012% (w/v) T4 in drinking water) thyroid rats in both clusters were supplemented orally with antioxidants (vitamin E or/and curcumin) for 30 days. Interactive least count difference and principal component analyses indicated increase in lipid peroxidation, reduced glutathione level, alteration in the activities and protein expression of antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase under altered thyroid states. However, the expression of stress survival molecules; nuclear factor κB (NFκB) and the serine-threonine kinase B (Akt), in hyper-thyroidism only points towards different mechanisms responsible for either condition. Co-administration of vitamin E and curcumin showed better result in attenuating expression of mammalian target for rapamycin (mTOR), restoration of total protein content and biological activity of Ca
2+
ATPase in hyperthyroid rats, whereas, their individual treatment showed partial restoration. Since NRF2 is responsible for activation of antioxidant response element and subsequent expression of antioxidant enzymes, possible interactions of both vitamin E or/and curcumin with the antioxidant enzymes, NRF2 and its regulator Kelch ECH associating protein (KEAP1) were studied
in silico
. For the first time, a modeled active portion of the zipped protein NRF2 indicated its interaction with both vitamin E and curcumin. Further, curcumin and vitamin E complex showed
in silico
interaction with KEAP1. Reduction of oxidative stress by curcumin and/or vitamin E may be due to modulation of NRF2 and KEAP1 function in rat heart under altered thyroid states.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31092832</pmid><doi>10.1038/s41598-019-43320-5</doi><orcidid>https://orcid.org/0000-0002-2969-0071</orcidid><orcidid>https://orcid.org/0000-0002-5285-6578</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Scientific reports, 2019-05, Vol.9 (1), p.7408, Article 7408 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6520394 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; Nature Free; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | 13/95 38/77 631/601/1332 64 692/4017 82/1 82/29 82/80 96/95 Adenosine triphosphatase AKT protein Animals Antioxidants Antioxidants - pharmacology Biological activity Blotting, Western Ca2+-transporting ATPase Calcium Calcium-Transporting ATPases - metabolism Catalase Curcumin Curcumin - pharmacology Drinking water Enzymes Glutathione peroxidase Glutathione reductase Heart Heart - drug effects Humanities and Social Sciences Hyperthyroidism Hyperthyroidism - metabolism Hypothyroidism Hypothyroidism - metabolism Kelch-Like ECH-Associated Protein 1 - metabolism Lipid peroxidation Lipid Peroxidation - drug effects Male multidisciplinary Myocardium - metabolism NF-E2-Related Factor 2 - metabolism NF-kappa B - metabolism NF-κB protein Oxidative stress Oxidative Stress - drug effects Peroxidation Propylthiouracil Protein-serine/threonine kinase Proteins Proto-Oncogene Proteins c-akt - metabolism Rapamycin Rats Rats, Wistar Science Science (multidisciplinary) Signal Transduction - drug effects Superoxide dismutase Thyroid Thyroid gland Thyroid Hormones - metabolism Vitamin E Vitamin E - pharmacology |
| title | Possible activation of NRF2 by Vitamin E/Curcumin against altered thyroid hormone induced oxidative stress via NFĸB/AKT/mTOR/KEAP1 signalling in rat heart |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T11%3A11%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Possible%20activation%20of%20NRF2%20by%20Vitamin%20E/Curcumin%20against%20altered%20thyroid%20hormone%20induced%20oxidative%20stress%20via%20NF%C4%B8B/AKT/mTOR/KEAP1%20signalling%20in%20rat%20heart&rft.jtitle=Scientific%20reports&rft.au=Mishra,%20Pallavi&rft.date=2019-05-15&rft.volume=9&rft.issue=1&rft.spage=7408&rft.pages=7408-&rft.artnum=7408&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-019-43320-5&rft_dat=%3Cproquest_pubme%3E2225813712%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2225813712&rft_id=info:pmid/31092832&rfr_iscdi=true |