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D-半乳糖胺诱导的细胞损伤增强前列腺素E1与大鼠肝细胞的特异性结合。

D-galactosamine-induced cell damage enhances specific binding of prostaglandin E1 to rat hepatocytes.

作者信息

Matsumoto M, Kikuchi E, Okamoto Y, Morimura M, Kitano H, Fukui H, Nakano H, Tsujii T

机构信息

Third Department of Internal Medicine, Nara Medical University, Japan.

出版信息

Biochem Biophys Res Commun. 1992 Apr 30;184(2):654-60. doi: 10.1016/0006-291x(92)90639-3.

DOI:10.1016/0006-291x(92)90639-3
PMID:1315527
Abstract

Specific bindings of [3H]prostaglandin E1 ([3H]PGE1), 125I-glucagon and [3H]norepinephrine to D-galactosamine (GalN)-treated rat hepatocytes in primary culture were investigated. After a two hour-treatment with GalN (1 and 10mg/ml), hepatocytes showed an enhanced specific binding to [3H]PGE1, whereas 125I-glucagon binding was little affected and [3H]norepinephrine binding was strongly diminished. Scatchard plot analysis indicated an increase of binding sites of [3H]PGE1. This unusual manner of [3H]PGE1 binding is suggested to indicate a special property of PGE1 receptor and may be associated with the cytoprotective effect of prostaglandins.

摘要

研究了[3H]前列腺素E1([3H]PGE1)、125I-胰高血糖素和[3H]去甲肾上腺素与原代培养的经D-半乳糖胺(GalN)处理的大鼠肝细胞的特异性结合。在用GalN(1和10mg/ml)处理两小时后,肝细胞对[3H]PGE1的特异性结合增强,而125I-胰高血糖素结合几乎未受影响,[3H]去甲肾上腺素结合则显著减少。Scatchard作图分析表明[3H]PGE1结合位点增加。这种[3H]PGE1结合的异常方式提示PGE1受体具有特殊性质,可能与前列腺素的细胞保护作用有关。

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