Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs
The anti-senescence activity of genistein is associated with inducing autophagy; however, the underlying mechanisms are not fully understood. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (1000 nM) for 30 min and then exposed to ox-LDL (50 mg/L) for an...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2019-05, Vol.455 (1-2), p.127-134 |
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| creator | Zhang, Huaping Yang, Xiaorong Pang, Xuefen Zhao, Zhenxiang Yu, Haixia Zhou, Hui |
| description | The anti-senescence activity of genistein is associated with inducing autophagy; however, the underlying mechanisms are not fully understood. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (1000 nM) for 30 min and then exposed to ox-LDL (50 mg/L) for another 12 h. The study found that genistein inhibited the ox-LDL-induced senescence (reducing the levels of P16 and P21 protein, and the activity of SA-β-gal); meanwhile, the effect of genistein was bound up with enhancing autophagic flux (increasing LC3-II, and decreasing the level of P62, p-mTOR and p-P70S6K). Moreover, SIRT1/LKB1/AMPK pathway was involved in genistein accelerating autophagic flux and mitigating senescence in HUVECs. The present study illustrated that genistein was a promising therapeutic agent to delay aging process and extend longevity. |
| doi_str_mv | 10.1007/s11010-018-3476-8 |
| format | Article |
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In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (1000 nM) for 30 min and then exposed to ox-LDL (50 mg/L) for another 12 h. The study found that genistein inhibited the ox-LDL-induced senescence (reducing the levels of P16 and P21 protein, and the activity of SA-β-gal); meanwhile, the effect of genistein was bound up with enhancing autophagic flux (increasing LC3-II, and decreasing the level of P62, p-mTOR and p-P70S6K). Moreover, SIRT1/LKB1/AMPK pathway was involved in genistein accelerating autophagic flux and mitigating senescence in HUVECs. The present study illustrated that genistein was a promising therapeutic agent to delay aging process and extend longevity.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-018-3476-8</identifier><identifier>PMID: 30443855</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aging ; AMP-Activated Protein Kinases - metabolism ; Angiogenesis inhibitors ; Autophagy ; Autophagy - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cellular Senescence - drug effects ; Chemical compounds ; Cilostazol ; Endothelial cells ; Endothelium ; Fluctuations ; Flux ; Genistein ; Genistein - pharmacology ; GTP-binding protein ; Human Umbilical Vein Endothelial Cells ; Humans ; Isoflavones ; Life Sciences ; Lipoproteins, LDL - pharmacology ; LKB1 protein ; Low density lipoprotein ; Low density lipoproteins ; Medical Biochemistry ; Oncology ; Phagocytosis ; Pharmacology ; Protein-Serine-Threonine Kinases - metabolism ; Proteins ; Senescence ; Signal Transduction - drug effects ; SIRT1 protein ; Sirtuin 1 - metabolism ; TOR protein ; Umbilical vein</subject><ispartof>Molecular and cellular biochemistry, 2019-05, Vol.455 (1-2), p.127-134</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2018</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Molecular and Cellular Biochemistry is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-e4379570c43abd1848b640ec3c528ea80373c1e5bb29ce2ce52a25c63042ff753</citedby><cites>FETCH-LOGICAL-c477t-e4379570c43abd1848b640ec3c528ea80373c1e5bb29ce2ce52a25c63042ff753</cites><orcidid>0000-0002-4002-7481</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/s11010-018-3476-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-018-3476-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30443855$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Huaping</creatorcontrib><creatorcontrib>Yang, Xiaorong</creatorcontrib><creatorcontrib>Pang, Xuefen</creatorcontrib><creatorcontrib>Zhao, Zhenxiang</creatorcontrib><creatorcontrib>Yu, Haixia</creatorcontrib><creatorcontrib>Zhou, Hui</creatorcontrib><title>Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>The anti-senescence activity of genistein is associated with inducing autophagy; however, the underlying mechanisms are not fully understood. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (1000 nM) for 30 min and then exposed to ox-LDL (50 mg/L) for another 12 h. The study found that genistein inhibited the ox-LDL-induced senescence (reducing the levels of P16 and P21 protein, and the activity of SA-β-gal); meanwhile, the effect of genistein was bound up with enhancing autophagic flux (increasing LC3-II, and decreasing the level of P62, p-mTOR and p-P70S6K). Moreover, SIRT1/LKB1/AMPK pathway was involved in genistein accelerating autophagic flux and mitigating senescence in HUVECs. The present study illustrated that genistein was a promising therapeutic agent to delay aging process and extend longevity.</description><subject>Aging</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Angiogenesis inhibitors</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cellular Senescence - drug effects</subject><subject>Chemical compounds</subject><subject>Cilostazol</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Fluctuations</subject><subject>Flux</subject><subject>Genistein</subject><subject>Genistein - pharmacology</subject><subject>GTP-binding protein</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Isoflavones</subject><subject>Life Sciences</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>LKB1 protein</subject><subject>Low density lipoprotein</subject><subject>Low density lipoproteins</subject><subject>Medical Biochemistry</subject><subject>Oncology</subject><subject>Phagocytosis</subject><subject>Pharmacology</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proteins</subject><subject>Senescence</subject><subject>Signal Transduction - drug effects</subject><subject>SIRT1 protein</subject><subject>Sirtuin 1 - metabolism</subject><subject>TOR protein</subject><subject>Umbilical vein</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc1u1DAUhSMEokPhAdigSGzYuOPrn7GzHIbSVg0CQcvWcpybjKuMM40Tafr29SgtSEjIC0v2d67P8cmy90DPgFK1jAAUKKGgCRdqRfSLbAFScSIKKF5mC8opJRqUOsnexHhHE0wBXmcnnArBtZSL7HCBwccRfcj3Qz-iG2NuW-tDHPP-QMovJfGhnhzWecSA0WFwmI_boZ_abY5ha4Pzoc1_Xf28gWV5_RmW628_rskOa2_HpLLT2O-3tn3Im2465Omdy9vf55v4NnvV2C7iu6f9NLv9en6zuSTl94urzbokTig1EhRcFVJRJ7itatBCVytB0XEnmUarKVfcAcqqYoVD5lAyy6RbpYSsaZTkp9mneW6Kdz9hHM3OpxRdZwP2UzQMuAQmgNGEfvwHveunISR3R4qv1JFM1NlMtbZD40PTj4N1adW4864P2Ph0vpYaqNaF5kkAs8ANfYwDNmY_-J0dHgxQc-zRzD2a1KM59mh00nx4sjJV6Sv_KJ6LSwCbgZiuQovDX6__n_oIkyimEg</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Zhang, Huaping</creator><creator>Yang, Xiaorong</creator><creator>Pang, Xuefen</creator><creator>Zhao, Zhenxiang</creator><creator>Yu, Haixia</creator><creator>Zhou, Hui</creator><general>Springer US</general><general>Springer</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</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>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4002-7481</orcidid></search><sort><creationdate>20190501</creationdate><title>Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs</title><author>Zhang, Huaping ; Yang, Xiaorong ; Pang, Xuefen ; Zhao, Zhenxiang ; Yu, Haixia ; Zhou, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-e4379570c43abd1848b640ec3c528ea80373c1e5bb29ce2ce52a25c63042ff753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aging</topic><topic>AMP-Activated Protein Kinases - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Huaping</au><au>Yang, Xiaorong</au><au>Pang, Xuefen</au><au>Zhao, Zhenxiang</au><au>Yu, Haixia</au><au>Zhou, Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>455</volume><issue>1-2</issue><spage>127</spage><epage>134</epage><pages>127-134</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The anti-senescence activity of genistein is associated with inducing autophagy; however, the underlying mechanisms are not fully understood. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (1000 nM) for 30 min and then exposed to ox-LDL (50 mg/L) for another 12 h. The study found that genistein inhibited the ox-LDL-induced senescence (reducing the levels of P16 and P21 protein, and the activity of SA-β-gal); meanwhile, the effect of genistein was bound up with enhancing autophagic flux (increasing LC3-II, and decreasing the level of P62, p-mTOR and p-P70S6K). Moreover, SIRT1/LKB1/AMPK pathway was involved in genistein accelerating autophagic flux and mitigating senescence in HUVECs. The present study illustrated that genistein was a promising therapeutic agent to delay aging process and extend longevity.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30443855</pmid><doi>10.1007/s11010-018-3476-8</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-4002-7481</orcidid></addata></record> |
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| subjects | Aging AMP-Activated Protein Kinases - metabolism Angiogenesis inhibitors Autophagy Autophagy - drug effects Biochemistry Biomedical and Life Sciences Cardiology Cellular Senescence - drug effects Chemical compounds Cilostazol Endothelial cells Endothelium Fluctuations Flux Genistein Genistein - pharmacology GTP-binding protein Human Umbilical Vein Endothelial Cells Humans Isoflavones Life Sciences Lipoproteins, LDL - pharmacology LKB1 protein Low density lipoprotein Low density lipoproteins Medical Biochemistry Oncology Phagocytosis Pharmacology Protein-Serine-Threonine Kinases - metabolism Proteins Senescence Signal Transduction - drug effects SIRT1 protein Sirtuin 1 - metabolism TOR protein Umbilical vein |
| title | Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs |
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