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仓鼠摄入鹅去氧胆酸后淀粉样变性增强。

Enhancement of amyloidosis by chenodeoxycholic acid ingestion in the hamster.

作者信息

Justrabo E, Olsson N O, Caignard A, Jeannin J F, Michiels R, Martin M

出版信息

Digestion. 1982;24(4):264-73. doi: 10.1159/000198807.

Abstract

A long-term experiment was performed to test the ability of chenodeoxycholic acid (CDCA) to induce intestinal tumors in the Syrian golden hamster. Animals were fed a CDCA-enriched diet up to 12 months, and 4 of them were sacrificed every 2 months. CDCA exhibited no carcinogenic activity. However, unexpected amyloid deposits were discovered in both treated and nontreated animals. Their incidence was significantly higher in treated (71%) than in nontreated (27%) hamsters. During CDCA administration, amyloidosis appeared as early as the second month of treatment. It involved the liver, spleen and kidneys in more than half of the animals. On the contrary, in control animals, amyloid deposits appeared later and were most frequently restricted to one organ. The intensity of the lesions also appeared to be greater in the treated group. No monoclonal components were found in either serum or urine of the amyloidotic hamsters. Such an amyloidosis-promoting effect of CDCA has never been reported.

摘要

进行了一项长期实验,以测试鹅去氧胆酸(CDCA)诱导叙利亚金黄地鼠肠道肿瘤的能力。给动物喂食富含CDCA的饮食长达12个月,每2个月处死4只动物。CDCA未表现出致癌活性。然而,在经处理和未经处理的动物中均发现了意外的淀粉样沉积物。其发生率在经处理的仓鼠(71%)中显著高于未经处理的仓鼠(27%)。在给予CDCA期间,淀粉样变性最早在治疗的第二个月出现。超过一半的动物肝脏、脾脏和肾脏受累。相反,在对照动物中,淀粉样沉积物出现较晚,且最常局限于一个器官。治疗组的病变强度似乎也更大。在淀粉样变性仓鼠的血清或尿液中均未发现单克隆成分。CDCA的这种促进淀粉样变性的作用从未有过报道。

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