Sulforaphane Inhibits MGO-AGE-Mediated Neuroinflammation by Suppressing NF-kappa B, MAPK, and AGE-RAGE Signaling Pathways in Microglial Cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Subedi, L. | - |
dc.contributor.author | Lee, J.H. | - |
dc.contributor.author | Gaire, B.P. | - |
dc.contributor.author | Kim, S.Y. | - |
dc.date.available | 2020-11-04T05:41:14Z | - |
dc.date.created | 2020-11-02 | - |
dc.date.issued | 2020-09 | - |
dc.identifier.issn | 2076-3921 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/78840 | - |
dc.description.abstract | Advanced glycation end products (AGEs) are produced through the binding of glycated protein or lipid with sugar, and they are known to be involved in the pathogenesis of both age-dependent and independent neurological complications. Among dicarbonyl compounds, methylglyoxal (MGO), which is produced from glucose breakdown, is a key precursor of AGE formation and neurotoxicity. Several studies have shown the toxic effects of bovine serum albumin (BSA)-AGE (prepared with glucose, sucrose or fructose) both in in vitro and in vivo. In fact, MGO-derived AGEs (MGO-AGEs) are highly toxic to neurons and other cells of the central nervous system. Therefore, we aimed to investigate the role of MGO-AGEs in microglial activation, a key inflammatory event, or secondary brain damage in neuroinflammatory diseases. Interestingly, we found that sulforaphane (SFN) as a potential candidate to downregulate neuroinflammation induced by MGO-AGEs in BV2 microglial cells. SFN not only inhibited the formation of MGO-AGEs, but it did not show breaking activity on the MGO-mediated AGEs cross-links with protein, indicating that SFN could potentially trap MGO or inhibit toxic AGE damage. In addition, SFN significantly attenuated the production of neuroinflammatory mediators induced by MGO-AGEs in BV2 microglial cells. SFN also lowered the expression levels of AGE receptor (RAGE) in microglial cells, suggesting that SFN could downregulate MGO-AGE-mediated neurotoxicity at the receptor activation level. Altogether, our current study revealed that SFN might show neuropharmacological potential for downregulating MGO-AGEs-mediated neuronal complications thorough attenuating AGE formation and neuroinflammatory responses induced by MGO-AGEs in vitro. © 2020 by the authors. Licensee MDPI, Basel, Switzerland. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI AG | - |
dc.relation.isPartOf | Antioxidants | - |
dc.title | Sulforaphane Inhibits MGO-AGE-Mediated Neuroinflammation by Suppressing NF-kappa B, MAPK, and AGE-RAGE Signaling Pathways in Microglial Cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000580695100001 | - |
dc.identifier.doi | 10.3390/antiox9090792 | - |
dc.identifier.bibliographicCitation | Antioxidants, v.9, no.9, pp.1 - 14 | - |
dc.identifier.scopusid | 2-s2.0-85093879330 | - |
dc.citation.endPage | 14 | - |
dc.citation.startPage | 1 | - |
dc.citation.title | Antioxidants | - |
dc.citation.volume | 9 | - |
dc.citation.number | 9 | - |
dc.contributor.affiliatedAuthor | Subedi, L. | - |
dc.contributor.affiliatedAuthor | Lee, J.H. | - |
dc.contributor.affiliatedAuthor | Gaire, B.P. | - |
dc.contributor.affiliatedAuthor | Kim, S.Y. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Advanced glycation end products | - |
dc.subject.keywordAuthor | Microglial activation | - |
dc.subject.keywordAuthor | Neuroinflammation | - |
dc.subject.keywordAuthor | Sulforaphane | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
1342, Seongnam-daero, Sujeong-gu, Seongnam-si, Gyeonggi-do, Republic of Korea(13120)031-750-5114
COPYRIGHT 2020 Gachon University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.