Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury
Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties....
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| Veröffentlicht in: | Neurochemical research 2023-03, Vol.48 (3), p.956-966 |
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| creator | Fan, Gui-bo Li, Yan Xu, Gao-shuo Zhao, A.-yang Jin, Hong-jiang Sun, Si-qi Qi, Si-hua |
| description | Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI. |
| doi_str_mv | 10.1007/s11064-022-03822-7 |
| format | Article |
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Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-022-03822-7</identifier><identifier>PMID: 36402927</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Accumulation ; Animals ; Anti-inflammatory agents ; Antioxidants ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Death ; Disease Models, Animal ; Ferroptosis ; Glutathione ; Inflammation ; Inhibitors ; Injuries ; Ischemia ; Lipid peroxidation ; Lipid Peroxides ; Lipids ; Mice ; Neurochemistry ; Neurology ; Neurons ; Neuroprotection ; Neurosciences ; NF-E2-Related Factor 2 ; Original Paper ; Peroxidation ; Peroxides ; Propofol ; Propofol - pharmacology ; Propofol - therapeutic use ; Reperfusion ; Reperfusion Injury - drug therapy ; Signal Transduction ; Signaling ; Transmission electron microscopy ; Western blotting</subject><ispartof>Neurochemical research, 2023-03, Vol.48 (3), p.956-966</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. 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Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.</description><subject>Accumulation</subject><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Death</subject><subject>Disease Models, Animal</subject><subject>Ferroptosis</subject><subject>Glutathione</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxides</subject><subject>Lipids</subject><subject>Mice</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2</subject><subject>Original Paper</subject><subject>Peroxidation</subject><subject>Peroxides</subject><subject>Propofol</subject><subject>Propofol - pharmacology</subject><subject>Propofol - therapeutic use</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Transmission electron microscopy</subject><subject>Western blotting</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9u1DAQxi0EotvCC3BAlrhwSTv-FydHtKWlUikVlHPkJOONV9k42Ilgb30BTrwhT1Jvt1CJA5cZaeY338zoI-QVg2MGoE8iY5DLDDjPQBQp6idkwZQWWV6CeEoWIFJbsBIOyGGMa4A0xtlzcpDqwEuuF-TndfCjt76nF0PnajdFeoYh1SY_uYYuse_pKZqpozdd8POqo1OH9CpYfnI-_pD0i1sNpnfDil4n6LvZUjfcIx_9HHexxZ56m4QC1sGkNbHpcOPM79tfn3HEYOfo_JC2r-ewfUGeWdNHfPmQj8jXs_c3yw_Z5afzi-W7y6wRWk2ZhCLXLRhpdSk4oOVto4QCyMtcYsFqjrWRxoLUqlENWstFY5lsVQtaGS2OyNu97hj8txnjVG1cbNKvZsB0d8W1KFhRasUT-uYfdO3nkH7eUVoJIVWRJ4rvqSb4GAPaagxuY8K2YlDtzKr2ZlXJrOrerGp3xesH6bneYPt35I87CRB7IKbWsMLwuPs_sndyAKCp</recordid><startdate>20230301</startdate><enddate>20230301</enddate><creator>Fan, Gui-bo</creator><creator>Li, Yan</creator><creator>Xu, Gao-shuo</creator><creator>Zhao, A.-yang</creator><creator>Jin, Hong-jiang</creator><creator>Sun, Si-qi</creator><creator>Qi, Si-hua</creator><general>Springer US</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20230301</creationdate><title>Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury</title><author>Fan, Gui-bo ; Li, Yan ; Xu, Gao-shuo ; Zhao, A.-yang ; Jin, Hong-jiang ; Sun, Si-qi ; Qi, Si-hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-40867d0a4f79320ef2dc535006964e81b2eba4af0475c5ceff23cf14d5d075a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Accumulation</topic><topic>Animals</topic><topic>Anti-inflammatory agents</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Death</topic><topic>Disease Models, Animal</topic><topic>Ferroptosis</topic><topic>Glutathione</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxides</topic><topic>Lipids</topic><topic>Mice</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>NF-E2-Related Factor 2</topic><topic>Original Paper</topic><topic>Peroxidation</topic><topic>Peroxides</topic><topic>Propofol</topic><topic>Propofol - 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Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, Gui-bo</au><au>Li, Yan</au><au>Xu, Gao-shuo</au><au>Zhao, A.-yang</au><au>Jin, Hong-jiang</au><au>Sun, Si-qi</au><au>Qi, Si-hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2023-03-01</date><risdate>2023</risdate><volume>48</volume><issue>3</issue><spage>956</spage><epage>966</epage><pages>956-966</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36402927</pmid><doi>10.1007/s11064-022-03822-7</doi><tpages>11</tpages></addata></record> |
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| subjects | Accumulation Animals Anti-inflammatory agents Antioxidants Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Cell Death Disease Models, Animal Ferroptosis Glutathione Inflammation Inhibitors Injuries Ischemia Lipid peroxidation Lipid Peroxides Lipids Mice Neurochemistry Neurology Neurons Neuroprotection Neurosciences NF-E2-Related Factor 2 Original Paper Peroxidation Peroxides Propofol Propofol - pharmacology Propofol - therapeutic use Reperfusion Reperfusion Injury - drug therapy Signal Transduction Signaling Transmission electron microscopy Western blotting |
| title | Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury |
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