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氨基氰诱导大鼠包涵体形成的回归机制:一种研究肝细胞β-糖原代谢的有用实验模式。

Regression mechanism of cyanamide-induced inclusion bodies in the rat: a useful experimental pattern to study the beta-glycogen metabolization of hepatocytes.

作者信息

Idoate M A, Vázquez J J

机构信息

Department of Pathology, University of Navarre, Pamplona, Spain.

出版信息

Int J Exp Pathol. 1992 Dec;73(6):699-708.

PMID:1337264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2002429/
Abstract

Cyanamide, a drug used in alcohol aversion therapy, induces a distinctive liver cell lesion, both in human beings and rats. The lesion consists of cytoplasmic inclusion bodies which give a ground-glass appearance to the hepatocytes. In human beings the inclusion bodies do not persist but disappear some time after withdrawal of the drug. In order to confirm their disappearance and determine how they regress rats were treated with cyanamide (32 mg/kg) for 6 months before partial lobectomy. At this time, inclusion bodies were observed. After a period without further treatment (5-19 weeks) the animals were killed and a marked decrease in the number of inclusion bodies was observed, paralleling the period of time without treatment. Inclusion bodies regress as a result of glycogen removal by enzymatic activity of the smooth endoplasmic reticulum which then undergoes hyperplasia, plus a process of autophagocytosis and necrosis of inclusion-body-bearing hepatocytes which are then phagocytosed by macrophages.

摘要

氨基氰是一种用于酒精厌恶疗法的药物,在人类和大鼠中都会引发一种独特的肝细胞病变。这种病变由细胞质包涵体组成,使肝细胞呈现出毛玻璃样外观。在人类中,包涵体不会持续存在,而是在停药后的一段时间内消失。为了证实它们的消失并确定其消退方式,在部分肝叶切除术前,用氨基氰(32毫克/千克)对大鼠进行了6个月的治疗。此时,观察到了包涵体。在未经进一步治疗的一段时间(5 - 19周)后,处死动物,观察到包涵体数量显著减少,这与未治疗的时间段平行。包涵体的消退是由于滑面内质网的酶活性去除糖原,随后滑面内质网增生,加上含包涵体的肝细胞发生自噬和坏死过程,然后被巨噬细胞吞噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/a7833f3b630f/ijexpath00024-0013-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/42c75b7d1c74/ijexpath00024-0009-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/9a141a5e23b3/ijexpath00024-0010-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/09355b258c8a/ijexpath00024-0011-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/c5e34bf408fa/ijexpath00024-0012-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/a7833f3b630f/ijexpath00024-0013-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/42c75b7d1c74/ijexpath00024-0009-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/9a141a5e23b3/ijexpath00024-0010-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/09355b258c8a/ijexpath00024-0011-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/c5e34bf408fa/ijexpath00024-0012-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/081d/2002429/a7833f3b630f/ijexpath00024-0013-a.jpg

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引用本文的文献

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本文引用的文献

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An electron microscope study of the early effects of 3'-Me-DAB on rat liver cells.3'-甲基二乙基亚硝胺对大鼠肝细胞早期影响的电子显微镜研究。
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Induction of focal hemopoiesis in adult rat liver by glucan, a macrophage activator. A cytochemical and ultrastructural study.巨噬细胞激活剂葡聚糖诱导成年大鼠肝脏局灶性造血:细胞化学与超微结构研究
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Drug therapy: Drugs to decrease alcohol consumption.药物治疗:用于减少酒精摄入量的药物。
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Cyanamide-induced liver injury. A predictable lesion.氰胺引起的肝损伤。一种可预测的病变。
Liver. 1983 Aug;3(4):225-30. doi: 10.1111/j.1600-0676.1983.tb00872.x.
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Cyanamide-induced liver cell injury. Experimental study in the rat.
Lab Invest. 1984 Apr;50(4):385-93.
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Ground glass inclusions in liver cells in an alcoholic treated with cyanamide (Dipsan).在用氨甲脒(迪普散)治疗的酒精性患者的肝细胞中出现磨玻璃样包涵体。
Liver. 1981 Mar;1(1):67-73. doi: 10.1111/j.1600-0676.1981.tb00024.x.
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Cyanamide-induced liver injury in alcoholics.酒精性患者中氨基氰诱发的肝损伤。
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The induction of drug-metabolizing enzymes in rat liver during growth and regeneration. A biochemical and ultrastructural study.
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A morphometric study of the removal of phenobarbital-induced membranes from hepatocytes after cessation of threatment.停药后从肝细胞中去除苯巴比妥诱导膜的形态计量学研究。
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Lack of hepatotoxicity after long-term administration of cyanamide in rats: a histological and biochemical study.大鼠长期服用氨基氰后的肝毒性缺失:一项组织学与生物化学研究
Acta Pharmacol Toxicol (Copenh). 1985 Oct;57(4):279-84. doi: 10.1111/j.1600-0773.1985.tb00043.x.