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首页> 外文期刊>The Journal of Nuclear Medicine >Increased technetium-99m-GSA uptake per hepatocyte in rats with administration of dimethylnitrosamine or hepatocyte growth factor.
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Increased technetium-99m-GSA uptake per hepatocyte in rats with administration of dimethylnitrosamine or hepatocyte growth factor.

机译:服用二甲基亚硝胺或肝细胞生长因子的大鼠每肝细胞对tech 99m-GSA的摄取增加。

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摘要

Technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin (GSA) is a new scintigraphic agent that binds specifically to asialoglycoprotein receptors on hepatocytes, and can be used to evaluate hepatic function. Asialoglycoprotein receptor is a hepatocellular membrane receptor responsible for the endocytosis of asialoglycoproteins, and the function of this receptor is affected in various disease states. The aim of this study was to investigate GSA uptake per hepatocyte in the convalescent stage from hepatic damage. METHODS: We used rats with dimethylnitrosamine (DMN)-induced hepatic injury and rats with recombinant human hepatocyte growth factor (rhHGF) stimulation. Plasma clearance of GSA and the number of hepatocytes in whole liver were calculated. RESULTS: In the DMN-treated rats, the total number of hepatocytes and GSA plasma clearance were reduced significantly at 3 wk after the final administration of DMN. However, calculated GSA uptake per individual hepatocyte was significantly greater by 53.2% than in the normal controls. The area of hepatic nucleus was also significantly greater than in the normal controls. In the rhHGF-treated rats, an increase in the total number of hepatocytes was not demonstrated on the final day of rhHGF administration (Day 4). However, calculated GSA uptake per hepatocyte was significantly greater (59%) than in the controls. CONCLUSION: Augmented GSA uptake per hepatocyte during the convalescent stage after hepatic injury suggests a cellular compensation to the decreased number of hepatocyte. This mechanism may be caused by the secretion of some hepatotropic factors such as HGF.
机译:m 99m-二亚乙基三胺五乙酸-半乳糖基-人血清白蛋白(GSA)是一种新型闪烁显像剂,可特异性结合肝细胞上的去唾液酸糖蛋白受体,可用于评估肝功能。去唾液酸糖蛋白受体是负责去唾液酸糖蛋白内吞作用的肝细胞膜受体,该受体的功能在各种疾病状态下都会受到影响。这项研究的目的是研究恢复期肝损伤后每个肝细胞对GSA的摄取。方法:我们使用了二甲基亚硝胺(DMN)诱导的肝损伤大鼠和重组人肝细胞生长因子(rhHGF)刺激的大鼠。计算了全肝中GSA的血浆清除率和肝细胞数量。结果:在DMN治疗的大鼠中,最后一次给予DMN后3周,肝细胞总数和GSA血浆清除率明显降低。但是,计算得出的每只肝细胞的GSA摄取量比正常对照组高53.2%。肝核的面积也明显大于正常对照。在rhHGF治疗的大鼠中,在rhHGF施用的最后一天(第4天)未证明肝细胞总数的增加。但是,计算得出的每肝细胞摄取GSA的比例(59%)明显高于对照组。结论:肝损伤后恢复期每肝细胞吸收GSA的增加提示细胞对肝细胞数量减少的补偿。此机制可能是由某些促肝因子(例如HGF)的分泌引起的。

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