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组织去甲肾上腺素耗竭作为半胱胺抑制Wistar大鼠中由氧化偶氮甲烷诱导的结肠癌发生的一种机制。

Tissue norepinephrine depletion as a mechanism for cysteamine inhibition of colon carcinogenesis induced by azoxymethane in Wistar rats.

作者信息

Tatsuta M, Iishi H, Baba M, Taniguchi H

机构信息

Department of Gastrointestinal Oncology, Center for Adult Diseases, Osaka, Japan.

出版信息

Int J Cancer. 1989 Dec 15;44(6):1008-11. doi: 10.1002/ijc.2910440612.

DOI:10.1002/ijc.2910440612
PMID:2606571
Abstract

The effects of cysteamine (2-aminoethanethiol hydrochloride) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the norepinephrine concentration in the colon wall tissue and the labelling indices of colon mucosa and colon cancers were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of AOM and alternate-day subcutaneous injections of 25 mg/kg of cysteamine in 0.9% NaCl solution until the end of the experiment. At week 40, prolonged administration of cysteamine significantly reduced the incidence and number of colon tumors. Histologically, the adenocarcinomas that did develop in rats treated with cysteamine exhibited high mucin-producing activity. Administration of cysteamine caused significant decreases in the norepinephrine concentration in colon tissue and in the labelling indices of colon mucosa and cancers. Our findings indicate that cysteamine inhibits the development of colon tumors. This action may be related to its effect in decreasing norepinephrine concentration in the colon wall tissues and subsequently in decreasing proliferation of colon cancer cells.

摘要

在Wistar大鼠中,研究了半胱胺(2-氨基乙硫醇盐酸盐)对由氧化偶氮甲烷(AOM)诱导的结肠肿瘤的发生率、数量和组织学的影响,以及对结肠壁组织中去甲肾上腺素浓度和结肠黏膜及结肠癌标记指数的影响。大鼠每周接受10次7.4mg/kg体重的AOM注射,并每隔一天皮下注射25mg/kg半胱胺于0.9%氯化钠溶液中,直至实验结束。在第40周时,长期给予半胱胺显著降低了结肠肿瘤的发生率和数量。组织学上,接受半胱胺治疗的大鼠中确实发生的腺癌表现出高粘蛋白产生活性。给予半胱胺导致结肠组织中去甲肾上腺素浓度以及结肠黏膜和癌症的标记指数显著降低。我们的研究结果表明,半胱胺抑制结肠肿瘤的发展。这种作用可能与其降低结肠壁组织中去甲肾上腺素浓度并随后降低结肠癌细胞增殖的作用有关。

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Tissue norepinephrine depletion as a mechanism for cysteamine inhibition of colon carcinogenesis induced by azoxymethane in Wistar rats.组织去甲肾上腺素耗竭作为半胱胺抑制Wistar大鼠中由氧化偶氮甲烷诱导的结肠癌发生的一种机制。
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