Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy
Oxidative stress is a critical factor in the pathology of age-related macular degeneration (AMD). Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat so...
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| creator | Hang, Li Li, Min Yu, Hai-tao Yang, Yan Zhang, Yuanzhong Xu, Xin-rong |
| description | Oxidative stress is a critical factor in the pathology of age-related macular degeneration (AMD). Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat solubility, which determines its low oral bioavailability. In this study, we prepared the solid dispersion of apigenin (AP-SD). The solubility and dissolution of AP-SD was significantly better than that of the original drug, so the oral bioavailability in rats was better than that of the original drug. Then, the effects of AP-SD on the retina of a model mouse with dry AMD were assessed by fundus autofluorescence (FAF), optical coherence tomography (OCT), and electron microscopy; the results revealed that AP-SD alleviated retinopathy. Further research found that AP-SD promoted the nuclear translocation of Nrf2 and increased expression levels of the Nrf2 and target genes HO-1 and NQO-1. AP-SD enhanced the activities of SOD and GSH-Px and decreased the levels of ROS and MDA. Furthermore, AP-SD upregulated the expressions of p62 and LC3II in an Nrf2-dependent manner. However, these effects of AP-SD were observed only in the retina of Nrf2 WT mice, not in Nrf2 KO mice. In addition, the therapeutic effect of AP-SD was dose dependent, and AP did not work. In conclusion, AP-SD significantly enhanced the bioavailability of the original drug and reduced retinal oxidative injury in the model mouse of dry AMD in vivo. The results of the underlying mechanism showed that AP-SD upregulated the expression of antioxidant enzymes through the Nrf2 pathway and upregulated autophagy, thus inhibiting retinal oxidative damage. AP-SD may be a potential compound for the treatment of dry AMD. |
| doi_str_mv | 10.1155/2020/9420704 |
| format | Article |
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Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat solubility, which determines its low oral bioavailability. In this study, we prepared the solid dispersion of apigenin (AP-SD). The solubility and dissolution of AP-SD was significantly better than that of the original drug, so the oral bioavailability in rats was better than that of the original drug. Then, the effects of AP-SD on the retina of a model mouse with dry AMD were assessed by fundus autofluorescence (FAF), optical coherence tomography (OCT), and electron microscopy; the results revealed that AP-SD alleviated retinopathy. Further research found that AP-SD promoted the nuclear translocation of Nrf2 and increased expression levels of the Nrf2 and target genes HO-1 and NQO-1. AP-SD enhanced the activities of SOD and GSH-Px and decreased the levels of ROS and MDA. Furthermore, AP-SD upregulated the expressions of p62 and LC3II in an Nrf2-dependent manner. However, these effects of AP-SD were observed only in the retina of Nrf2 WT mice, not in Nrf2 KO mice. In addition, the therapeutic effect of AP-SD was dose dependent, and AP did not work. In conclusion, AP-SD significantly enhanced the bioavailability of the original drug and reduced retinal oxidative injury in the model mouse of dry AMD in vivo. The results of the underlying mechanism showed that AP-SD upregulated the expression of antioxidant enzymes through the Nrf2 pathway and upregulated autophagy, thus inhibiting retinal oxidative damage. AP-SD may be a potential compound for the treatment of dry AMD.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/9420704</identifier><identifier>PMID: 32509154</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Aging ; Analysis ; Animals ; Antioxidants ; Antioxidants - therapeutic use ; Apigenin - therapeutic use ; Autophagy ; Bioavailability ; Bioflavonoids ; Cells, Cultured ; Disease Models, Animal ; Drugs ; Ethanol ; Fatty acids ; Flavones ; Flavonoids ; Flow velocity ; Homeostasis ; Humans ; Macular degeneration ; Macular Degeneration - drug therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Oxidative Stress ; Plasma ; Povidone ; Rats ; Rats, Sprague-Dawley ; Retina - metabolism ; Retina - pathology ; Signal Transduction</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-14</ispartof><rights>Copyright © 2020 Yuanzhong Zhang et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Yuanzhong Zhang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Yuanzhong Zhang et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-5078f450486a9c651a3c6c8007e78810d954f189373efd7ad7d3959f7118baf23</citedby><cites>FETCH-LOGICAL-c499t-5078f450486a9c651a3c6c8007e78810d954f189373efd7ad7d3959f7118baf23</cites><orcidid>0000-0003-2047-7298</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/PMC7244986/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244986/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32509154$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mendonça Junior, Francisco Jaime B.</contributor><contributor>Francisco Jaime B Mendonça Junior</contributor><creatorcontrib>Hang, Li</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Yu, Hai-tao</creatorcontrib><creatorcontrib>Yang, Yan</creatorcontrib><creatorcontrib>Zhang, Yuanzhong</creatorcontrib><creatorcontrib>Xu, Xin-rong</creatorcontrib><title>Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Oxidative stress is a critical factor in the pathology of age-related macular degeneration (AMD). Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat solubility, which determines its low oral bioavailability. In this study, we prepared the solid dispersion of apigenin (AP-SD). The solubility and dissolution of AP-SD was significantly better than that of the original drug, so the oral bioavailability in rats was better than that of the original drug. Then, the effects of AP-SD on the retina of a model mouse with dry AMD were assessed by fundus autofluorescence (FAF), optical coherence tomography (OCT), and electron microscopy; the results revealed that AP-SD alleviated retinopathy. Further research found that AP-SD promoted the nuclear translocation of Nrf2 and increased expression levels of the Nrf2 and target genes HO-1 and NQO-1. AP-SD enhanced the activities of SOD and GSH-Px and decreased the levels of ROS and MDA. Furthermore, AP-SD upregulated the expressions of p62 and LC3II in an Nrf2-dependent manner. However, these effects of AP-SD were observed only in the retina of Nrf2 WT mice, not in Nrf2 KO mice. In addition, the therapeutic effect of AP-SD was dose dependent, and AP did not work. In conclusion, AP-SD significantly enhanced the bioavailability of the original drug and reduced retinal oxidative injury in the model mouse of dry AMD in vivo. The results of the underlying mechanism showed that AP-SD upregulated the expression of antioxidant enzymes through the Nrf2 pathway and upregulated autophagy, thus inhibiting retinal oxidative damage. AP-SD may be a potential compound for the treatment of dry AMD.</description><subject>Aging</subject><subject>Analysis</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - therapeutic use</subject><subject>Apigenin - therapeutic use</subject><subject>Autophagy</subject><subject>Bioavailability</subject><subject>Bioflavonoids</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Drugs</subject><subject>Ethanol</subject><subject>Fatty acids</subject><subject>Flavones</subject><subject>Flavonoids</subject><subject>Flow velocity</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Macular degeneration</subject><subject>Macular Degeneration - drug therapy</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative Stress</subject><subject>Plasma</subject><subject>Povidone</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Retina - metabolism</subject><subject>Retina - pathology</subject><subject>Signal Transduction</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0c9v0zAUB_AIgdgY3DgjS1yQWLfnH7HjC1I12EAabEJwtl4TO_GUOiV2Nvrfz1VLxzhx8pP90df2e0XxmsIJpWV5yoDBqRYMFIgnxSHN5Qy0Fk_3NcBB8SLGGwDJmaDPiwPOStC0FIdFM1_51gYfyPU4JFunSL4OU7Tku00-IMEWfYiJXP32DSZ_a8lHXGJryWKdSTv1eTO0JHWWfBsdI9eYujtcEwwNmU9pWHXYrl8Wzxz20b7arUfFz_NPP84-zy6vLr6czS9ntdA6zUpQlRMliEqirmVJkdeyrgCUVVVFodGlcLTSXHHrGoWNargutVOUVgt0jB8VH7a5q2mxtE1tQxqxN6vRL3FcmwG9eXwSfGfa4dYoJoSuZA54twsYh1-Tjcksfaxt32OwuSsmdy-3mVMOmb79h94M0xjy97ICyRQDKh9Ui701Prgh31tvQs1csooqxaTO6nir6nGIcbRu_2QKZjNksxmy2Q058zd_f3OP_0w1g_db0PnQ4J3_zzibjXX4oBlIEJrfA9QVtq0</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Hang, Li</creator><creator>Li, Min</creator><creator>Yu, Hai-tao</creator><creator>Yang, Yan</creator><creator>Zhang, Yuanzhong</creator><creator>Xu, Xin-rong</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2047-7298</orcidid></search><sort><creationdate>2020</creationdate><title>Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy</title><author>Hang, Li ; Li, Min ; Yu, Hai-tao ; Yang, Yan ; Zhang, Yuanzhong ; Xu, Xin-rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-5078f450486a9c651a3c6c8007e78810d954f189373efd7ad7d3959f7118baf23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Analysis</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - therapeutic use</topic><topic>Apigenin - therapeutic use</topic><topic>Autophagy</topic><topic>Bioavailability</topic><topic>Bioflavonoids</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Drugs</topic><topic>Ethanol</topic><topic>Fatty acids</topic><topic>Flavones</topic><topic>Flavonoids</topic><topic>Flow velocity</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Macular degeneration</topic><topic>Macular Degeneration - drug therapy</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative Stress</topic><topic>Plasma</topic><topic>Povidone</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Retina - metabolism</topic><topic>Retina - pathology</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hang, Li</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Yu, Hai-tao</creatorcontrib><creatorcontrib>Yang, Yan</creatorcontrib><creatorcontrib>Zhang, Yuanzhong</creatorcontrib><creatorcontrib>Xu, Xin-rong</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hang, Li</au><au>Li, Min</au><au>Yu, Hai-tao</au><au>Yang, Yan</au><au>Zhang, Yuanzhong</au><au>Xu, Xin-rong</au><au>Mendonça Junior, Francisco Jaime B.</au><au>Francisco Jaime B Mendonça Junior</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>14</epage><pages>1-14</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Oxidative stress is a critical factor in the pathology of age-related macular degeneration (AMD). Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat solubility, which determines its low oral bioavailability. In this study, we prepared the solid dispersion of apigenin (AP-SD). The solubility and dissolution of AP-SD was significantly better than that of the original drug, so the oral bioavailability in rats was better than that of the original drug. Then, the effects of AP-SD on the retina of a model mouse with dry AMD were assessed by fundus autofluorescence (FAF), optical coherence tomography (OCT), and electron microscopy; the results revealed that AP-SD alleviated retinopathy. Further research found that AP-SD promoted the nuclear translocation of Nrf2 and increased expression levels of the Nrf2 and target genes HO-1 and NQO-1. AP-SD enhanced the activities of SOD and GSH-Px and decreased the levels of ROS and MDA. Furthermore, AP-SD upregulated the expressions of p62 and LC3II in an Nrf2-dependent manner. However, these effects of AP-SD were observed only in the retina of Nrf2 WT mice, not in Nrf2 KO mice. In addition, the therapeutic effect of AP-SD was dose dependent, and AP did not work. In conclusion, AP-SD significantly enhanced the bioavailability of the original drug and reduced retinal oxidative injury in the model mouse of dry AMD in vivo. The results of the underlying mechanism showed that AP-SD upregulated the expression of antioxidant enzymes through the Nrf2 pathway and upregulated autophagy, thus inhibiting retinal oxidative damage. AP-SD may be a potential compound for the treatment of dry AMD.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32509154</pmid><doi>10.1155/2020/9420704</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-2047-7298</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aging Analysis Animals Antioxidants Antioxidants - therapeutic use Apigenin - therapeutic use Autophagy Bioavailability Bioflavonoids Cells, Cultured Disease Models, Animal Drugs Ethanol Fatty acids Flavones Flavonoids Flow velocity Homeostasis Humans Macular degeneration Macular Degeneration - drug therapy Mice Mice, Inbred C57BL Mice, Knockout NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Oxidative Stress Plasma Povidone Rats Rats, Sprague-Dawley Retina - metabolism Retina - pathology Signal Transduction |
| title | Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy |
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