期刊
NEUROSCIENCE LETTERS
卷 444, 期 3, 页码 264-269出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2008.08.057
关键词
Baicalein; Hypoxia; BV2 microglia; HIF-1 alpha; PI 3-kinase; ROS
资金
- Korea Science and Engineering Foundation [R13-2002-020-02001-0]
- National Research Foundation of Korea [R13-2002-020-02001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Hypoxia induces an inflammatory activation of microglia during cerebral ischemia. The transcription factor of hypoxia-inducible genes hypoxia-inducible factor-1 (HIF-1) is known to be involved in inflammation and immune response. Although baicalein (BE), a flavonoid, is shown to have anti-inflammatory effects and attenuate ischemic injury, its action mechanism is not understood well. Thus, we examined effect of BE on hypoxia-induced HIF-1 activation and its signaling mechanism in BV2 microglial cells. BE inhibited hypoxia-induced HIF-1 alpha protein accumulation and HIF-1 transcriptional activation. Consistently, BE suppressed hypoxia-induced expression of hypoxia responsive genes, NOS, COX-2, and VEGF. We then showed that BE inhibited hypoxia-induced phosphorylation of Akt but not that of ERK and p38. Moreover, BE inhibited hypoxia-incluced PI 3-kinase activation. Finally,we showed that BE inhibited hypoxia-incluced ROS generation, and an antioxidant N-acetylcysteine reduced hypoxia-induced HIF-1 alpha and NOS protein expression and PI 3-kinase/Akt activation in BV2 microglia. Taken together, these results suggest that BE suppresses hypoxia-incluced HIF-1 alpha protein and activation as well as expression of hypoxia responsive genes by inhibiting ROS and PI 3-kinase/Akt pathway in BV2 microglia. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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