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- Publisher Website: 10.1007/s12035-018-1027-7
- Scopus: eid_2-s2.0-85045035520
- PMID: 29627876
- WOS: WOS:000448483400019
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Article: Naringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation
Title | Naringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation |
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Authors | |
Keywords | Cerebral ischemia-reperfusion injury Mitophagy Naringin Nitrative stress Peroxynitrite |
Issue Date | 2018 |
Publisher | Humana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035 |
Citation | Molecular Neurobiology, 2018, v. 55 n. 12, p. 9029-9042 How to Cite? |
Abstract | Excessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO−), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO−-mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO− scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO− donor 3-morpholinosydnonimine conditions. Naringin also inhibited the expression of NADPH oxidase subunits and iNOS in rat brains subjected to 2 h ischemia plus 22 h reperfusion. Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. Furthermore, naringin reduced 3-nitrotyrosine formation, decreased the ratio of LC3-II to LC3-I in mitochondrial fraction, and inhibited the translocation of Parkin to the mitochondria. Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO−-mediated excessive mitophagy. |
Persistent Identifier | http://hdl.handle.net/10722/261815 |
ISSN | 2021 Impact Factor: 5.682 2020 SCImago Journal Rankings: 1.569 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Feng, J | - |
dc.contributor.author | Chen, X | - |
dc.contributor.author | Lu, S | - |
dc.contributor.author | Li, W | - |
dc.contributor.author | Yang, D | - |
dc.contributor.author | Su, W | - |
dc.contributor.author | Wang, X | - |
dc.contributor.author | Shen, J | - |
dc.date.accessioned | 2018-09-28T04:48:34Z | - |
dc.date.available | 2018-09-28T04:48:34Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Molecular Neurobiology, 2018, v. 55 n. 12, p. 9029-9042 | - |
dc.identifier.issn | 0893-7648 | - |
dc.identifier.uri | http://hdl.handle.net/10722/261815 | - |
dc.description.abstract | Excessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO−), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO−-mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO− scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO− donor 3-morpholinosydnonimine conditions. Naringin also inhibited the expression of NADPH oxidase subunits and iNOS in rat brains subjected to 2 h ischemia plus 22 h reperfusion. Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. Furthermore, naringin reduced 3-nitrotyrosine formation, decreased the ratio of LC3-II to LC3-I in mitochondrial fraction, and inhibited the translocation of Parkin to the mitochondria. Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO−-mediated excessive mitophagy. | - |
dc.language | eng | - |
dc.publisher | Humana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035 | - |
dc.relation.ispartof | Molecular Neurobiology | - |
dc.rights | The final publication is available at Springer via http://dx.doi.org/[insert DOI] | - |
dc.subject | Cerebral ischemia-reperfusion injury | - |
dc.subject | Mitophagy | - |
dc.subject | Naringin | - |
dc.subject | Nitrative stress | - |
dc.subject | Peroxynitrite | - |
dc.title | Naringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation | - |
dc.type | Article | - |
dc.identifier.email | Yang, D: yangdan@hku.hk | - |
dc.identifier.email | Shen, J: shenjg@hku.hk | - |
dc.identifier.authority | Yang, D=rp00825 | - |
dc.identifier.authority | Shen, J=rp00487 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1007/s12035-018-1027-7 | - |
dc.identifier.pmid | 29627876 | - |
dc.identifier.scopus | eid_2-s2.0-85045035520 | - |
dc.identifier.hkuros | 292992 | - |
dc.identifier.volume | 55 | - |
dc.identifier.issue | 12 | - |
dc.identifier.spage | 9029 | - |
dc.identifier.epage | 9042 | - |
dc.identifier.isi | WOS:000448483400019 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0893-7648 | - |