2026-03-11T13:02:54Z https://kanazawa-u.repo.nii.ac.jp/oai

oai:kanazawa-u.repo.nii.ac.jp:00015229 2024-06-27T01:20:15Z 4281:4291:4312

Anti-inflammatory effects of lipoic acid through inhibition of GSK-3β in lipopolysaccharide-induced BV-2 microglial cells 郡山, 恵樹 松郷, 誠一 杉谷, 加代 大貝, 和裕 高寺, 恒雄 加藤, 聖 Koriyama, Yoshiki 332 70397199 70397199 Nakayama, Yuya 27526 Matsugo, Seiichi 311 30148126 30148126 30148126 Sugitani, Kayo 371 20162258 20162258 Ogai, Kazuhiro 23291 40706983 Takadera, Tsuneo 1555 90121277 90121277 Kato, Satoru 72 10019614 10019614 Activated microglial cells play an important role in immune and inflammatory responses in CNS and play a role in neurodegenerative diseases. We examined the effects of lipoic acid (LA) on inflammatory responses of BV-2 microglial cells activated by lipopolysaccharide (LPS), and explored the underlying mechanisms of action of LA. BV-2 cells treated with LPS showed an up-regulation of mRNA of the pro-inflammatory molecules, inducible nitric oxide synthase (iNOS). LA suppressed the expression of iNOS and furthermore, LPS-induced production of nitrite. Moreover, LA suppressed the nuclear translocation of RelA, a component of nuclear factor-kappa B (NF-κB) that contains transcriptional activator domain for LPS. The mechanisms of LA-mediated anti-inflammatory effects on microglia remain unknown, and we suggested an involvement of Akt/glycogen synthase kinase-3β (GSK-3β) phosphorylation. The results showed that inhibitor of phosphatidylinositol 3-kinase prevented LA-mediated suppression of LPS induction of RelA and expression of iNOS. Furthermore, these inflammatory actions were prevented by GSK-3β inhibitors. These data demonstrate a role for LA as a chemical modulator of inflammatory responses by microglia, and thus may be a therapeutic strategy for treating neurodegenerative diseases with an inflammatory component. © 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. journal article Elsevier 2013-09-01 AM application/pdf Neuroscience Research 1-2 77 87 96 AA10641652 0168-0102 https://kanazawa-u.repo.nii.ac.jp/record/15229/files/ME-PR-KORIYAMA-Y-87.pdf https://doi.org/10.24517/00015216 http://hdl.handle.net/2297/36255 https://kanazawa-u.repo.nii.ac.jp/records/15229 eng 10.1016/j.neures.2013.07.001 http://www.elsevier.com/locate/issn/01680102