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缺氧在肝星状细胞激活中的作用机制

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摘要 目的:探讨缺氧在肝星状细胞(HSC)激活中的作用机制。方法:缺氧培养大鼠HSC株HSC-T6,逆转录PCR检测HIF-1α、TGF-β1、I型胶原mRNA的表达,Westren blot检测α-SMA表达。缺氧/常氧下,加TGF-β1中和抗体、HIF-1α诱导剂氯化钴(CoCl2)或抑制剂2-甲氧雌二醇(2ME2),逆转录PCR检测HSC-T6表达I型胶原mRNA的变化。结果:缺氧能诱导HSC-T6表达HIF-1α、TGF-β1、I型胶原mRNA及α-SMA蛋白;常氧下CoCl2能诱导HSC-T6表达I型胶原mR-NA,TGF-β1中和抗体及2ME2能减弱缺氧诱导HSC-T6表达I型胶原mRNA,但表达量仍高于常氧培养。结论:缺氧能激活HSC,分泌I型胶原,增加细胞外基质沉积,其作用机制既依赖于TGF-β的胞内信号传导机制,也与HIF-α介导的信号传导有关,在肝纤维化形成中起着举足轻重的作用。
作者 邓毅恒 窦科峰 张福琴 李俊杰
机构地区 第四军医大学西京医院肝胆外科
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2010年第5期487-489,共3页 Chinese Journal of Cellular and Molecular Immunology
关键词 缺氧 转化生长因子-1β 缺氧诱导因子-1Α 肝星状细胞 肝纤维化
分类号 R575.22 [医药卫生—消化系统]
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参考文献10

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细胞与分子免疫学杂志
2010年 第5期

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