Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells
An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Eda...
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| creator | Li, Yanwei Liu, Haifeng Zeng, Wei Wei, Jing |
| description | An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC. |
| doi_str_mv | 10.1371/journal.pone.0174437 |
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Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0174437</identifier><identifier>PMID: 28346481</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenosine Triphosphate - metabolism ; Antipyrine - analogs & derivatives ; Antipyrine - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Atherosclerosis ; Biology and Life Sciences ; Caspase ; Caspase 3 - metabolism ; Caspase-3 ; Cell death ; Clinical medicine ; Cornea ; Cytochrome ; Cytochrome c ; Disease ; Dosage and administration ; Edaravone ; Epidemiology ; Epithelial cells ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelium, Corneal - cytology ; Epithelium, Corneal - drug effects ; Epithelium, Corneal - metabolism ; Evaporation ; Eye ; Fluorides ; Free Radical Scavengers - pharmacology ; Free radicals ; Health aspects ; Hospitals ; Humans ; Hydroxyl radicals ; Ischemia ; Kinases ; Laboratories ; Medicine and Health Sciences ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Membranes ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Neuroprotective agents ; Osmolar Concentration ; Osmolarity ; Osmotic pressure ; Otolaryngology ; Oxidative stress ; Oxidative Stress - drug effects ; Protective Agents - pharmacology ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Research and Analysis Methods ; Rodents ; Stroke ; Tears ; Toxicity</subject><ispartof>PloS one, 2017-03, Vol.12 (3), p.e0174437</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Li et al 2017 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-612b543c3764cdbb4df34f4bf575b79ee967a3d4c1720e3cd80b904d849ca37e3</citedby><cites>FETCH-LOGICAL-c758t-612b543c3764cdbb4df34f4bf575b79ee967a3d4c1720e3cd80b904d849ca37e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5367814/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5367814/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23870,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28346481$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Reddy, Hemachandra</contributor><creatorcontrib>Li, Yanwei</creatorcontrib><creatorcontrib>Liu, Haifeng</creatorcontrib><creatorcontrib>Zeng, Wei</creatorcontrib><creatorcontrib>Wei, Jing</creatorcontrib><title>Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Antipyrine - analogs & derivatives</subject><subject>Antipyrine - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Atherosclerosis</subject><subject>Biology and Life Sciences</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell death</subject><subject>Clinical medicine</subject><subject>Cornea</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Disease</subject><subject>Dosage and administration</subject><subject>Edaravone</subject><subject>Epidemiology</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelium, Corneal - cytology</subject><subject>Epithelium, Corneal - drug effects</subject><subject>Epithelium, Corneal - metabolism</subject><subject>Evaporation</subject><subject>Eye</subject><subject>Fluorides</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Free radicals</subject><subject>Health aspects</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hydroxyl radicals</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Medicine and Health Sciences</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Membranes</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Neuroprotective agents</subject><subject>Osmolar Concentration</subject><subject>Osmolarity</subject><subject>Osmotic pressure</subject><subject>Otolaryngology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Protective Agents - pharmacology</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Stroke</subject><subject>Tears</subject><subject>Toxicity</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk19r2zAUxc3YWLts32BshsHYHpJZlmzZL4NSui1QKOzfq7iWrhMFR3IlObTsy09p3BKPPgw_WEi_cyQd3Zskr0m2IJSTTxs7OAPdorcGFxnhjFH-JDklNc3nZZ7Rp0fjk-SF95ssK2hVls-Tk7yirGQVOU3-XChwsIseae9sQBl8CivQxod0fdujs35rO3A63M61UYNEldobrSDoHaY-OPRRYFQKve2D9dqn2kQrvQV3m66HLZhUWmcQuhR7HdbY6TiU2HX-ZfKshc7jq_E_S359ufh5_m1-efV1eX52OZe8qMK8JHlTMCopL5lUTcNUS1nLmrbgRcNrxLrkQBWThOcZUqmqrKkzpipWS6Ac6Sx5e_DtO-vFmJsXpKryvGQspjRLlgdCWdiI8fTCghZ3E9atBLigZYeCNFBzVVcgG2RQYw20kjkUBW9ISymPXp_H3YZmi0qiCQ66iel0xei1WNmdKGjJK8KiwYfRwNnrAX0QW-33gYFBO9ydm_D43GUW0Xf_oI_fbqRWEC-gTWvjvnJvKs5YxWlkGI3U4hEqfgq3WsYCaXWcnwg-TgSRCXgTVjB4L5Y_vv8_e_V7yr4_YtexcsLa224I2ho_BdkBlLFKvcP2IWSSiX2P3Kch9j0ixh6JsjfHD_Qgum8K-hfaWQ-b</recordid><startdate>20170327</startdate><enddate>20170327</enddate><creator>Li, Yanwei</creator><creator>Liu, Haifeng</creator><creator>Zeng, Wei</creator><creator>Wei, Jing</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170327</creationdate><title>Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells</title><author>Li, Yanwei ; Liu, Haifeng ; Zeng, Wei ; Wei, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-612b543c3764cdbb4df34f4bf575b79ee967a3d4c1720e3cd80b904d849ca37e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Antipyrine - analogs & derivatives</topic><topic>Antipyrine - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Atherosclerosis</topic><topic>Biology and Life Sciences</topic><topic>Caspase</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell death</topic><topic>Clinical medicine</topic><topic>Cornea</topic><topic>Cytochrome</topic><topic>Cytochrome c</topic><topic>Disease</topic><topic>Dosage and administration</topic><topic>Edaravone</topic><topic>Epidemiology</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelium, Corneal - cytology</topic><topic>Epithelium, Corneal - drug effects</topic><topic>Epithelium, Corneal - metabolism</topic><topic>Evaporation</topic><topic>Eye</topic><topic>Fluorides</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Free radicals</topic><topic>Health aspects</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Hydroxyl radicals</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Medicine and Health Sciences</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Membranes</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Neuroprotective agents</topic><topic>Osmolar Concentration</topic><topic>Osmolarity</topic><topic>Osmotic pressure</topic><topic>Otolaryngology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Protective Agents - pharmacology</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Research and Analysis Methods</topic><topic>Rodents</topic><topic>Stroke</topic><topic>Tears</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yanwei</creatorcontrib><creatorcontrib>Liu, Haifeng</creatorcontrib><creatorcontrib>Zeng, Wei</creatorcontrib><creatorcontrib>Wei, Jing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yanwei</au><au>Liu, Haifeng</au><au>Zeng, Wei</au><au>Wei, Jing</au><au>Reddy, Hemachandra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-03-27</date><risdate>2017</risdate><volume>12</volume><issue>3</issue><spage>e0174437</spage><pages>e0174437-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28346481</pmid><doi>10.1371/journal.pone.0174437</doi><tpages>e0174437</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adenosine Triphosphate - metabolism Antipyrine - analogs & derivatives Antipyrine - pharmacology Apoptosis Apoptosis - drug effects Atherosclerosis Biology and Life Sciences Caspase Caspase 3 - metabolism Caspase-3 Cell death Clinical medicine Cornea Cytochrome Cytochrome c Disease Dosage and administration Edaravone Epidemiology Epithelial cells Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelium, Corneal - cytology Epithelium, Corneal - drug effects Epithelium, Corneal - metabolism Evaporation Eye Fluorides Free Radical Scavengers - pharmacology Free radicals Health aspects Hospitals Humans Hydroxyl radicals Ischemia Kinases Laboratories Medicine and Health Sciences Membrane potential Membrane Potential, Mitochondrial - drug effects Membranes Mitochondria Mitochondria - drug effects Mitochondria - metabolism Neuroprotective agents Osmolar Concentration Osmolarity Osmotic pressure Otolaryngology Oxidative stress Oxidative Stress - drug effects Protective Agents - pharmacology Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Research and Analysis Methods Rodents Stroke Tears Toxicity |
| title | Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T11%3A26%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Edaravone%20protects%20against%20hyperosmolarity-induced%20oxidative%20stress%20and%20apoptosis%20in%20primary%20human%20corneal%20epithelial%20cells&rft.jtitle=PloS%20one&rft.au=Li,%20Yanwei&rft.date=2017-03-27&rft.volume=12&rft.issue=3&rft.spage=e0174437&rft.pages=e0174437-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0174437&rft_dat=%3Cgale_plos_%3EA487341943%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1882264419&rft_id=info:pmid/28346481&rft_galeid=A487341943&rft_doaj_id=oai_doaj_org_article_1ba97d98acbe4a9e9a38c2a557b1f337&rfr_iscdi=true |