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Translocation of Bax in rat hepatocytes cultured with ferric nitrilotriacetate

机译:次氮基三乙酸铁培养的大鼠肝细胞中Bax的易位

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Hepatic fibrosis occurs after many years of iron overload in liver. An effective iron deposition model induced by ferric nitrilotriacetate (FeNTA) in cultured rat hepatocytes was assumed. It has been shown that treatment of rat hepatocytes with FeNTA lead to oxidative stress and hepatocyte apoptosis. Hepatocyte apoptosis can promote liver fibrosis. The mechanisms of hepatocyte apoptosis induced by FeNTA have not yet been fully elucidated. The present stud), demonstrated that FeNTA-induced hepatocyte apoptosis was related to Bax translocation, cytochrome c release, and caspase-3 activation. (c) 2005 Published by Elsevier Inc.
机译:肝中铁超载多年后,就会发生肝纤维化。假定由次氮基三乙酸铁(FeNTA)在培养的大鼠肝细胞中诱导了有效的铁沉积模型。已经显示用FeNTA处理大鼠肝细胞导致氧化应激和肝细胞凋亡。肝细胞凋亡可促进肝纤维化。 FeNTA诱导肝细​​胞凋亡的机制尚未完全阐明。本研究表明,FeNTA诱导的肝细胞凋亡与Bax易位,细胞色素c释放和caspase-3激活有关。 (c)2005年由Elsevier Inc.发布。

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