@article{oai:kanazawa-u.repo.nii.ac.jp:00015229,
 author = {郡山, 恵樹 and 松郷, 誠一 and 杉谷, 加代 and 大貝, 和裕 and 高寺, 恒雄 and 加藤, 聖 and Koriyama, Yoshiki and Nakayama, Yuya and Matsugo, Seiichi and Sugitani, Kayo and Ogai, Kazuhiro and Takadera, Tsuneo and Kato, Satoru},
 issue = {1-2},
 journal = {Neuroscience Research},
 month = {Sep},
 note = {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.},
 pages = {87--96},
 title = {Anti-inflammatory effects of lipoic acid through inhibition of GSK-3β in lipopolysaccharide-induced BV-2 microglial cells},
 volume = {77},
 year = {2013}
}