Liproxstatin-1 Protects Hair Cell-Like HEI-OC1 Cells and Cochlear Hair Cells against Neomycin Ototoxicity
Ferroptosis is a recently discovered iron-dependent form of oxidative programmed cell death distinct from caspase-dependent apoptosis. In this study, we investigated the effect of ferroptosis in neomycin-induced hair cell loss by using selective ferroptosis inhibitor liproxstatin-1 (Lip-1). Cell via...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2020, Vol.2020 (2020), p.1-15 |
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| creator | He, Yingzi Hu, Bing Han, Jinghong Li, Wen Zhao, Liping Tang, Dongmei Zheng, Zhiwei Nie, Guohui |
| description | Ferroptosis is a recently discovered iron-dependent form of oxidative programmed cell death distinct from caspase-dependent apoptosis. In this study, we investigated the effect of ferroptosis in neomycin-induced hair cell loss by using selective ferroptosis inhibitor liproxstatin-1 (Lip-1). Cell viability was identified by CCK8 assay. The levels of reactive oxygen species (ROS) were determined by DCFH-DA and cellROX green staining. The mitochondrial membrane potential (ΔΨm) was evaluated by TMRM staining. Intracellular iron and lipid peroxides were detected with Mito-FerroGreen and Liperfluo probes. We found that ferroptosis can be induced in both HEI-OC1 cells and neonatal mouse cochlear explants, as evidenced by Mito-FerroGreen and Liperfluo staining. Further experiments showed that pretreatment with Lip-1 significantly alleviated neomycin-induced increased ROS generation and disruption in ΔΨm in the HEI-OC1 cells. In parallel, Lip-1 significantly attenuated neomycin-induced hair cell damage in neonatal mouse cochlear explants. Collectively, these results suggest a novel mechanism for neomycin-induced ototoxicity and suggest that ferroptosis inhibition may be a new clinical intervention to prevent hearing loss. |
| doi_str_mv | 10.1155/2020/1782659 |
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In this study, we investigated the effect of ferroptosis in neomycin-induced hair cell loss by using selective ferroptosis inhibitor liproxstatin-1 (Lip-1). Cell viability was identified by CCK8 assay. The levels of reactive oxygen species (ROS) were determined by DCFH-DA and cellROX green staining. The mitochondrial membrane potential (ΔΨm) was evaluated by TMRM staining. Intracellular iron and lipid peroxides were detected with Mito-FerroGreen and Liperfluo probes. We found that ferroptosis can be induced in both HEI-OC1 cells and neonatal mouse cochlear explants, as evidenced by Mito-FerroGreen and Liperfluo staining. Further experiments showed that pretreatment with Lip-1 significantly alleviated neomycin-induced increased ROS generation and disruption in ΔΨm in the HEI-OC1 cells. In parallel, Lip-1 significantly attenuated neomycin-induced hair cell damage in neonatal mouse cochlear explants. Collectively, these results suggest a novel mechanism for neomycin-induced ototoxicity and suggest that ferroptosis inhibition may be a new clinical intervention to prevent hearing loss.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/1782659</identifier><identifier>PMID: 33343803</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antibodies ; Apoptosis ; Cell culture ; Cell Line ; Experiments ; Flow cytometry ; Hair Cells, Auditory - metabolism ; Hair Cells, Auditory - pathology ; Hearing loss ; Ischemia ; Lipids ; Mice ; Morphology ; Neomycin - adverse effects ; Neomycin - pharmacology ; Ototoxicity - metabolism ; Ototoxicity - pathology ; Ototoxicity - prevention & control ; Oxidative stress ; Proteins ; Quinoxalines - pharmacology ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Spiro Compounds - pharmacology</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-15</ispartof><rights>Copyright © 2020 Zhiwei Zheng et al.</rights><rights>Copyright © 2020 Zhiwei Zheng 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. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Zhiwei Zheng et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-1f419f8f3d3aa7a5d1e3608962d14c5ac51a9e74becb2096de876d149f2a0f093</citedby><cites>FETCH-LOGICAL-c471t-1f419f8f3d3aa7a5d1e3608962d14c5ac51a9e74becb2096de876d149f2a0f093</cites><orcidid>0000-0001-7050-8094 ; 0000-0001-9414-4934 ; 0000-0002-6472-3799 ; 0000-0001-8996-345X ; 0000-0003-2756-2030 ; 0000-0003-0943-6831 ; 0000-0002-2248-2237</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/PMC7725559/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725559/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33343803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Muntean, Danina</contributor><contributor>Danina Muntean</contributor><creatorcontrib>He, Yingzi</creatorcontrib><creatorcontrib>Hu, Bing</creatorcontrib><creatorcontrib>Han, Jinghong</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Zhao, Liping</creatorcontrib><creatorcontrib>Tang, Dongmei</creatorcontrib><creatorcontrib>Zheng, Zhiwei</creatorcontrib><creatorcontrib>Nie, Guohui</creatorcontrib><title>Liproxstatin-1 Protects Hair Cell-Like HEI-OC1 Cells and Cochlear Hair Cells against Neomycin Ototoxicity</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Ferroptosis is a recently discovered iron-dependent form of oxidative programmed cell death distinct from caspase-dependent apoptosis. In this study, we investigated the effect of ferroptosis in neomycin-induced hair cell loss by using selective ferroptosis inhibitor liproxstatin-1 (Lip-1). Cell viability was identified by CCK8 assay. The levels of reactive oxygen species (ROS) were determined by DCFH-DA and cellROX green staining. The mitochondrial membrane potential (ΔΨm) was evaluated by TMRM staining. Intracellular iron and lipid peroxides were detected with Mito-FerroGreen and Liperfluo probes. We found that ferroptosis can be induced in both HEI-OC1 cells and neonatal mouse cochlear explants, as evidenced by Mito-FerroGreen and Liperfluo staining. Further experiments showed that pretreatment with Lip-1 significantly alleviated neomycin-induced increased ROS generation and disruption in ΔΨm in the HEI-OC1 cells. In parallel, Lip-1 significantly attenuated neomycin-induced hair cell damage in neonatal mouse cochlear explants. 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In this study, we investigated the effect of ferroptosis in neomycin-induced hair cell loss by using selective ferroptosis inhibitor liproxstatin-1 (Lip-1). Cell viability was identified by CCK8 assay. The levels of reactive oxygen species (ROS) were determined by DCFH-DA and cellROX green staining. The mitochondrial membrane potential (ΔΨm) was evaluated by TMRM staining. Intracellular iron and lipid peroxides were detected with Mito-FerroGreen and Liperfluo probes. We found that ferroptosis can be induced in both HEI-OC1 cells and neonatal mouse cochlear explants, as evidenced by Mito-FerroGreen and Liperfluo staining. Further experiments showed that pretreatment with Lip-1 significantly alleviated neomycin-induced increased ROS generation and disruption in ΔΨm in the HEI-OC1 cells. In parallel, Lip-1 significantly attenuated neomycin-induced hair cell damage in neonatal mouse cochlear explants. Collectively, these results suggest a novel mechanism for neomycin-induced ototoxicity and suggest that ferroptosis inhibition may be a new clinical intervention to prevent hearing loss.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33343803</pmid><doi>10.1155/2020/1782659</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-7050-8094</orcidid><orcidid>https://orcid.org/0000-0001-9414-4934</orcidid><orcidid>https://orcid.org/0000-0002-6472-3799</orcidid><orcidid>https://orcid.org/0000-0001-8996-345X</orcidid><orcidid>https://orcid.org/0000-0003-2756-2030</orcidid><orcidid>https://orcid.org/0000-0003-0943-6831</orcidid><orcidid>https://orcid.org/0000-0002-2248-2237</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Apoptosis Cell culture Cell Line Experiments Flow cytometry Hair Cells, Auditory - metabolism Hair Cells, Auditory - pathology Hearing loss Ischemia Lipids Mice Morphology Neomycin - adverse effects Neomycin - pharmacology Ototoxicity - metabolism Ototoxicity - pathology Ototoxicity - prevention & control Oxidative stress Proteins Quinoxalines - pharmacology Reactive oxygen species Reactive Oxygen Species - metabolism Spiro Compounds - pharmacology |
| title | Liproxstatin-1 Protects Hair Cell-Like HEI-OC1 Cells and Cochlear Hair Cells against Neomycin Ototoxicity |
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