{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T14:00:56Z","timestamp":1791900056021,"version":"4.3.4"},"reference-count":55,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2020,8,26]],"date-time":"2020-08-26T00:00:00Z","timestamp":1598400000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, and Forestry (IPET)","award":["318027-04-2-HD030"],"award-info":[{"award-number":["318027-04-2-HD030"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.3390\/antiox9090792","type":"journal-article","created":{"date-parts":[[2020,8,26]],"date-time":"2020-08-26T09:56:58Z","timestamp":1598435818000},"page":"792","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Sulforaphane Inhibits MGO-AGE-Mediated Neuroinflammation by Suppressing NF-\u03baB, MAPK, and AGE\u2013RAGE Signaling Pathways in Microglial Cells"],"prefix":"10.3390","volume":"9","author":[{"given":"Lalita","family":"Subedi","sequence":"first","affiliation":[{"name":"College of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4304-0198","authenticated-orcid":false,"given":"Jae Hyuk","family":"Lee","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bhakta Prasad","family":"Gaire","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8044-5613","authenticated-orcid":false,"given":"Sun Yeou","family":"Kim","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea"},{"name":"Gachon Institute of Pharmaceutical Science, Gachon University, #191 Hambakmoe-ro, Yeonsu-gu, Incheon 21936, Korea"},{"name":"Gachon Medical Research Institute, Gil Medical Center, Incheon 21565, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,8,26]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"911","DOI":"10.1016\/j.jada.2010.03.018","article-title":"Advanced glycation end products in foods and a practical guide to their reduction in the diet","volume":"110","author":"Uribarri","year":"2010","journal-title":"J. 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