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  会員専用

• ホーム
• 51巻11号
• 臨床神経, 51：1032−1035, 2011
• 51巻11号目次

＜シンポジウム19―2＞グリア細胞と神経疾患

脳虚血とアストロサイト

��橋　愼一

慶應義塾大学医学部神経内科〔〒160―8582 東京都新宿区信濃町35〕

Reactive oxygen species (ROS) derived from mitochondria in neural cells play an essential role in the pathophysiology of stroke. Hyperglycemia is also known to enhance ROS production, resulting in oxidative stress. We reported that both acute and chronic high glucose environments enhance the pentose phosphate pathway (PPP) in astroglia, reducing ROS production and thereby providing a neuroprotective role. In particular, chronic hyperglycemia elicits PPP activation through the Keap1/Nrf2 system, which is induced by endoplasmic (ER) stress via an increase in hexosamine biosynthetic pathway flux. We examined the effects of hypoxia with or without glucoprivation on PPP in cultured neurons and astroglia. Hypoxia without glucoprivation for 12 or 24 hours induced PPP activation in astroglia (126% and 177%, respectively) but not in neurons. PPP activation by hypoxia was accompanied by Nrf2 translocation to the nucleus but not by Bip expression in the ER. Re-oxygenation supplemented with glucose after 12 hours of hypoxia with or without glucoprivation markedly enhanced PPP in astroglia (231% and 178%, respectively). Hypoxia induced PPP activation in astroglia, exerting a neuroprotective role. While the Keap1/Nrf2 system seems to be involved, ER stress is not necessarily required.
Full Text of this Article in Japanese PDF (271K)

(臨床神経, 51：1032−1035, 2011)
key words：脳梗塞，アストログリア，活性酸素種，ペントースリン酸経路，Keap1/Nrf2システム

（受付日：2011年5月20日）