Sulforaphane Inhibits MGO-AGE-Mediated Neuroinflammation by Suppressing NF-kappa B, MAPK, and AGE-RAGE Signaling Pathways in Microglial Cells
- Authors
- Subedi, L.; Lee, J.H.; Gaire, B.P.; Kim, S.Y.
- Issue Date
- Sep-2020
- Publisher
- MDPI AG
- Keywords
- Advanced glycation end products; Microglial activation; Neuroinflammation; Sulforaphane
- Citation
- Antioxidants, v.9, no.9, pp.1 - 14
- Journal Title
- Antioxidants
- Volume
- 9
- Number
- 9
- Start Page
- 1
- End Page
- 14
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/78840
- DOI
- 10.3390/antiox9090792
- ISSN
- 2076-3921
- 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.
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