Therapeutic potential of coenzyme Q10 in mitochondrial dysfunction during tacrolimus-induced beta cell injury
We previously reported that oxidative stress induced by long-term tacrolimus treatment impairs mitochondrial function in pancreatic beta cells. In this study, we aimed to investigate the therapeutic potential of coenzyme Q 10 , which is known to be a powerful antioxidant, in mitochondrial dysfunctio...
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creator | Luo, Kang Yu, Ji Hyun Quan, Yi Shin, Yoo Jin Lee, Kyung Eun Kim, Hong Lim Ko, Eun Jeong Chung, Byung Ha Lim, Sun Woo Yang, Chul Woo |
description | We previously reported that oxidative stress induced by long-term tacrolimus treatment impairs mitochondrial function in pancreatic beta cells. In this study, we aimed to investigate the therapeutic potential of coenzyme Q
10
, which is known to be a powerful antioxidant, in mitochondrial dysfunction in tacrolimus-induced diabetic rats. In a rat model of tacrolimus-induced diabetes mellitus, coenzyme Q
10
treatment improved pancreatic beta cell function. The administration of coenzyme Q
10
improved insulin immunoreactivity within islets, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that coenzyme Q
10
treatment increased the size, number, and volume of mitochondria, as well as the number of insulin granules compared with that induced by tacrolimus treatment alone. An
in vitro
study using a pancreatic beta cell line showed that tacrolimus treatment increased apoptosis and the production of mitochondrial reactive oxygen species, while cotreatment with coenzyme Q
10
effectively attenuated these alterations. At the subcellular level, tacrolimus-induced impairment of mitochondrial respiration was significantly improved by coenzyme Q
10
, as evidenced by the increased mitochondrial oxygen consumption and ATP production. Our data indicate that coenzyme Q
10
plays an important role in reducing tacrolimus-induced oxidative stress and protects the mitochondria in pancreatic beta cells. These findings suggest that supplementation with coenzyme Q
10
has beneficial effects in tacrolimus-induced diabetes mellitus. |
doi_str_mv | 10.1038/s41598-019-44475-x |
format | Article |
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10
, which is known to be a powerful antioxidant, in mitochondrial dysfunction in tacrolimus-induced diabetic rats. In a rat model of tacrolimus-induced diabetes mellitus, coenzyme Q
10
treatment improved pancreatic beta cell function. The administration of coenzyme Q
10
improved insulin immunoreactivity within islets, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that coenzyme Q
10
treatment increased the size, number, and volume of mitochondria, as well as the number of insulin granules compared with that induced by tacrolimus treatment alone. An
in vitro
study using a pancreatic beta cell line showed that tacrolimus treatment increased apoptosis and the production of mitochondrial reactive oxygen species, while cotreatment with coenzyme Q
10
effectively attenuated these alterations. At the subcellular level, tacrolimus-induced impairment of mitochondrial respiration was significantly improved by coenzyme Q
10
, as evidenced by the increased mitochondrial oxygen consumption and ATP production. Our data indicate that coenzyme Q
10
plays an important role in reducing tacrolimus-induced oxidative stress and protects the mitochondria in pancreatic beta cells. These findings suggest that supplementation with coenzyme Q
10
has beneficial effects in tacrolimus-induced diabetes mellitus.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-44475-x</identifier><identifier>PMID: 31142763</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14/63 ; 692/4022/272 ; 692/699/317 ; 96/2 ; 96/31 ; Antioxidants ; Apoptosis ; Beta cells ; Cell injury ; Coenzyme Q10 ; Diabetes ; Diabetes mellitus ; Electron microscopy ; Electron transport ; Glucose ; Humanities and Social Sciences ; Immunoreactivity ; Insulin ; Mitochondria ; multidisciplinary ; Oxidative stress ; Oxygen consumption ; Pancreas ; Reactive oxygen species ; Science ; Science (multidisciplinary) ; Supplements ; Tacrolimus ; Ultrastructure</subject><ispartof>Scientific reports, 2019-05, Vol.9 (1), Article 7995</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-c488t-fef9207ed4261eecbe89ca4d816c817e39dd7fe10a7d930a8589ea24e4fff6c03</citedby><cites>FETCH-LOGICAL-c488t-fef9207ed4261eecbe89ca4d816c817e39dd7fe10a7d930a8589ea24e4fff6c03</cites><orcidid>0000-0003-4616-9955 ; 0000-0003-0048-5717</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/PMC6541596/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6541596/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids></links><search><creatorcontrib>Luo, Kang</creatorcontrib><creatorcontrib>Yu, Ji Hyun</creatorcontrib><creatorcontrib>Quan, Yi</creatorcontrib><creatorcontrib>Shin, Yoo Jin</creatorcontrib><creatorcontrib>Lee, Kyung Eun</creatorcontrib><creatorcontrib>Kim, Hong Lim</creatorcontrib><creatorcontrib>Ko, Eun Jeong</creatorcontrib><creatorcontrib>Chung, Byung Ha</creatorcontrib><creatorcontrib>Lim, Sun Woo</creatorcontrib><creatorcontrib>Yang, Chul Woo</creatorcontrib><title>Therapeutic potential of coenzyme Q10 in mitochondrial dysfunction during tacrolimus-induced beta cell injury</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><description>We previously reported that oxidative stress induced by long-term tacrolimus treatment impairs mitochondrial function in pancreatic beta cells. In this study, we aimed to investigate the therapeutic potential of coenzyme Q
10
, which is known to be a powerful antioxidant, in mitochondrial dysfunction in tacrolimus-induced diabetic rats. In a rat model of tacrolimus-induced diabetes mellitus, coenzyme Q
10
treatment improved pancreatic beta cell function. The administration of coenzyme Q
10
improved insulin immunoreactivity within islets, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that coenzyme Q
10
treatment increased the size, number, and volume of mitochondria, as well as the number of insulin granules compared with that induced by tacrolimus treatment alone. An
in vitro
study using a pancreatic beta cell line showed that tacrolimus treatment increased apoptosis and the production of mitochondrial reactive oxygen species, while cotreatment with coenzyme Q
10
effectively attenuated these alterations. At the subcellular level, tacrolimus-induced impairment of mitochondrial respiration was significantly improved by coenzyme Q
10
, as evidenced by the increased mitochondrial oxygen consumption and ATP production. Our data indicate that coenzyme Q
10
plays an important role in reducing tacrolimus-induced oxidative stress and protects the mitochondria in pancreatic beta cells. These findings suggest that supplementation with coenzyme Q
10
has beneficial effects in tacrolimus-induced diabetes mellitus.</description><subject>14/63</subject><subject>692/4022/272</subject><subject>692/699/317</subject><subject>96/2</subject><subject>96/31</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Beta cells</subject><subject>Cell injury</subject><subject>Coenzyme Q10</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Electron microscopy</subject><subject>Electron transport</subject><subject>Glucose</subject><subject>Humanities and Social Sciences</subject><subject>Immunoreactivity</subject><subject>Insulin</subject><subject>Mitochondria</subject><subject>multidisciplinary</subject><subject>Oxidative stress</subject><subject>Oxygen consumption</subject><subject>Pancreas</subject><subject>Reactive oxygen species</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Supplements</subject><subject>Tacrolimus</subject><subject>Ultrastructure</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>BENPR</sourceid><recordid>eNp9kU9rFTEUxUOptKX2C7gKuJ6afzOTbAQpWoWCCHUd8pKbvjxmkjHJSF8_vXm-UnVjNjdwz_kl9x6E3lByTQmX74qgvZIdoaoTQox993iCLhgRfcc4Y6d_3c_RVSk70k7PlKDqDJ1zSgUbB36B5vstZLPAWoPFS6oQazATTh7bBPFpPwP-RgkOEc-hJrtN0eWDwO2LX6OtIUXs1hziA67G5jSFeS1diG614PAGqsEWpqkBdmvev0avvJkKXD3XS_T908f7m8_d3dfbLzcf7jorpKydB68YGcEJNlAAuwGprBFO0sFKOgJXzo0eKDGjU5wY2UsFhgkQ3vvBEn6J3h-5y7qZwdk2VTaTXnKYTd7rZIL-txPDVj-kn3roD2sdGuDtMyCnHyuUqndpzbH9WTPGqRqVZLKp2FHVBi8lg395gRJ9SEkfU9ItJf07Jf3YTPxoKsthbZD_oP_j-gXqGpgr</recordid><startdate>20190529</startdate><enddate>20190529</enddate><creator>Luo, Kang</creator><creator>Yu, Ji Hyun</creator><creator>Quan, Yi</creator><creator>Shin, Yoo Jin</creator><creator>Lee, Kyung Eun</creator><creator>Kim, Hong Lim</creator><creator>Ko, Eun Jeong</creator><creator>Chung, Byung Ha</creator><creator>Lim, Sun Woo</creator><creator>Yang, Chul Woo</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</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>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4616-9955</orcidid><orcidid>https://orcid.org/0000-0003-0048-5717</orcidid></search><sort><creationdate>20190529</creationdate><title>Therapeutic potential of coenzyme Q10 in mitochondrial dysfunction during tacrolimus-induced beta cell injury</title><author>Luo, Kang ; 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In this study, we aimed to investigate the therapeutic potential of coenzyme Q
10
, which is known to be a powerful antioxidant, in mitochondrial dysfunction in tacrolimus-induced diabetic rats. In a rat model of tacrolimus-induced diabetes mellitus, coenzyme Q
10
treatment improved pancreatic beta cell function. The administration of coenzyme Q
10
improved insulin immunoreactivity within islets, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that coenzyme Q
10
treatment increased the size, number, and volume of mitochondria, as well as the number of insulin granules compared with that induced by tacrolimus treatment alone. An
in vitro
study using a pancreatic beta cell line showed that tacrolimus treatment increased apoptosis and the production of mitochondrial reactive oxygen species, while cotreatment with coenzyme Q
10
effectively attenuated these alterations. At the subcellular level, tacrolimus-induced impairment of mitochondrial respiration was significantly improved by coenzyme Q
10
, as evidenced by the increased mitochondrial oxygen consumption and ATP production. Our data indicate that coenzyme Q
10
plays an important role in reducing tacrolimus-induced oxidative stress and protects the mitochondria in pancreatic beta cells. These findings suggest that supplementation with coenzyme Q
10
has beneficial effects in tacrolimus-induced diabetes mellitus.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31142763</pmid><doi>10.1038/s41598-019-44475-x</doi><orcidid>https://orcid.org/0000-0003-4616-9955</orcidid><orcidid>https://orcid.org/0000-0003-0048-5717</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 14/63 692/4022/272 692/699/317 96/2 96/31 Antioxidants Apoptosis Beta cells Cell injury Coenzyme Q10 Diabetes Diabetes mellitus Electron microscopy Electron transport Glucose Humanities and Social Sciences Immunoreactivity Insulin Mitochondria multidisciplinary Oxidative stress Oxygen consumption Pancreas Reactive oxygen species Science Science (multidisciplinary) Supplements Tacrolimus Ultrastructure |
title | Therapeutic potential of coenzyme Q10 in mitochondrial dysfunction during tacrolimus-induced beta cell injury |
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