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内毒素对大鼠肝细胞清蛋白基因表达的影响 被引量:1

Response of albumin synthesis to lipopolysaccharide in rat hepatocytes
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摘要 目的 :观察内毒素刺激后体外培养大鼠肝细胞清蛋白基因的表达 ,进一步了解感染时低清蛋白血症的分子机制。 方法 :将 1 μg/ml内毒素作用于大鼠肝细胞后 0、2、8、1 2、2 4h ,分别用逆转录聚合酶链反应 (RT PCR)、流式细胞仪和酶链免疫检测法 (EIA) ,检测肝细胞清蛋白mRNA、细胞质内清蛋白前体和分泌到细胞外的清蛋白变化。 结果 :肝细胞清蛋白mRNA、细胞质内清蛋白前体和分泌到细胞外的清蛋白的变化是一致的 ,即内毒素作用后 2和 8h下降不明显 ,1 2h开始下降 ,2 4h后明显下降。清蛋白mRNA降低约 30 % ,清蛋白前体和清蛋白均下降5 0 %。 结论 :内毒素可以在体外抑制大鼠肝细胞清蛋白基因的表达 。 Objectives: To investigate the response of albumin synthesis in rat hepatocytes in vitro in early acute phase of LPS challenge. Methods: There were two groups of three samples randomizedto receive either normal saline or 1μg/L LPS. The albumin mRNA in hepatocytes was assessed and the albumin in the supernatantwas measured at 0, 2, 8, 12, 24 h after treatment. Meanwhile, the albumin precursorwas evaluated at the same time points with flow metric analysis. Results: The quantitative changes of mRNA, albumin precursor and its protein wereanalogous.All of them became to decline at 12 h post treatment and did not decrease significantly until 24 h after LPS challenge. Meanwhile, albumin mRNA decreased about 30% and the levels of albumin precursorand albuminreduced approximately 50%. Conclusions: LPS can inhibit the albumin synthesis of hepatocytes by prevention of albumintranscription. Moreover, the response of hepatic albumin synthesis to LPS changes with the stage of sepsis process and the other mechanisms are responsible for the hypoalbuminaemia syndrome.
出处 《肠外与肠内营养》 CAS 2004年第3期139-142,共4页 Parenteral & Enteral Nutrition
基金 全军"十五"医学科研基金重点课题 (批准号 :0 1Z0 11) 江苏省青年科技基金 (批准号 :BK9915 8)资助项目
关键词 内毒素 大鼠 肝细胞 清蛋白基因 基因表达 分子机制 Lipopolysaccharide Hepatocyte Albumin Hypoalbuminemia Sepsis
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