• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

灰黄霉素诱导瑞士白化小鼠胆汁淤积。

Griseofulvin-induced cholestasis in Swiss albino mice.

作者信息

Yokoo H, Craig R M, Harwood T R, Cochrane C

出版信息

Gastroenterology. 1979 Nov;77(5):1082-7.

PMID:488635
Abstract

Griseofulvin was fed to male Swiss albino mice, which were sacrificed at varying times after the initiation of the feeding. The following were compared with mice fed a control diet: hepatic histology, hepatic weight, plasma glycocholate, glycolithocholate, cholesterol, bilirubin, and alkaline phosphatase. Concurrent with the development of hepatic protoporphyria, a progressive cholestatic lesion was produced with marked bile canalicular dilatation and elevation of the plasma bile salts, alkaline phosphatase, and cholesterol without a rise in bilirubin. Adaptation to the cholestatic injury occurred in about 60 days despite continued griseofulvin feeding. This was evidenced by decreased values in the biochemical profile with concomitant improvement in the bile canalicular morphology. Following this event of adaptation, Mallory bodies began to appear in the livers, often in the periphery of the hepatic lobule. This model may be useful in studying mechanisms of cholestasis, Mallory body formation, and their relationship to altered microtubular systems in the hepatocyte.

摘要

将灰黄霉素喂给雄性瑞士白化小鼠,在开始喂食后的不同时间将其处死。将以下各项与喂食对照饮食的小鼠进行比较:肝脏组织学、肝脏重量、血浆甘氨胆酸盐、甘氨石胆酸盐、胆固醇、胆红素和碱性磷酸酶。随着肝脏原卟啉症的发展,出现了进行性胆汁淤积性病变,伴有明显的胆小管扩张以及血浆胆汁盐、碱性磷酸酶和胆固醇升高,而胆红素未升高。尽管持续喂食灰黄霉素,但在约60天时出现了对胆汁淤积性损伤的适应。这表现为生化指标值降低,同时胆小管形态有所改善。在这种适应事件之后,马洛小体开始出现在肝脏中,通常位于肝小叶周边。该模型可能有助于研究胆汁淤积的机制、马洛小体的形成及其与肝细胞中微管系统改变的关系。

相似文献

1
Griseofulvin-induced cholestasis in Swiss albino mice.灰黄霉素诱导瑞士白化小鼠胆汁淤积。
Gastroenterology. 1979 Nov;77(5):1082-7.
2
Experimental production of Mallory bodies in mice by diet containing 3,5-diethoxycarbonyl-1,4-dihydrocollidine.
Gastroenterology. 1982 Jul;83(1 Pt 1):109-13.
3
Effects of diosgenin, a plant-derived steroid, on bile secretion and hepatocellular cholestasis induced by estrogens in the rat.植物源性甾体化合物薯蓣皂苷元对大鼠雌激素诱导的胆汁分泌及肝细胞性胆汁淤积的影响。
Hepatology. 1998 Jul;28(1):129-40. doi: 10.1002/hep.510280118.
4
NTP technical report on the toxicity studies of Dibutyl Phthalate (CAS No. 84-74-2) Administered in Feed to F344/N Rats and B6C3F1 Mice.美国国家毒理学计划关于邻苯二甲酸二丁酯(化学物质登记号84 - 74 - 2)经饲料给予F344/N大鼠和B6C3F1小鼠的毒性研究技术报告。
Toxic Rep Ser. 1995 Apr;30:1-G5.
5
Effect of ursodeoxycholic acid on experimental hepatic porphyria induced by griseofulvin.熊去氧胆酸对灰黄霉素诱导的实验性肝卟啉症的影响。
J Korean Med Sci. 1991 Jun;6(2):146-56. doi: 10.3346/jkms.1991.6.2.146.
6
Relationship of Mallory bodies to the cytoskeleton of hepatocytes in griseofulvin-treated mice.灰黄霉素处理小鼠中马洛里小体与肝细胞细胞骨架的关系。
Lab Invest. 1982 Oct;47(4):336-45.
7
Rearrangement of the hepatocyte cytoskeleton after toxic damage: involution, dispersal and peripheral accumulation of Mallory body material after drug withdrawal.毒性损伤后肝细胞细胞骨架的重排:停药后马洛里小体物质的退化、分散和外周聚集。
Eur J Cell Biol. 1981 Feb;23(2):241-9.
8
Structural and functional alterations of hepatocytes during transient phalloidin-induced cholestasis in the rat.大鼠短暂性鬼笔环肽诱导胆汁淤积期间肝细胞的结构和功能改变
Toxicol Appl Pharmacol. 1996 Mar;137(1):100-11. doi: 10.1006/taap.1996.0061.
9
Hepatic gene expression in protoporphyic Fech mice is associated with cholestatic injury but not a marked depletion of the heme regulatory pool.原卟啉症Fech小鼠的肝脏基因表达与胆汁淤积性损伤相关,但与血红素调节池的显著消耗无关。
Am J Pathol. 2005 Apr;166(4):1041-53. doi: 10.1016/S0002-9440(10)62325-5.
10
Impaired activity of the bile canalicular organic anion transporter (Mrp2/cmoat) is not the main cause of ethinylestradiol-induced cholestasis in the rat.胆小管有机阴离子转运体(Mrp2/cmoat)活性受损并非乙炔雌二醇诱导大鼠胆汁淤积的主要原因。
Hepatology. 1998 Feb;27(2):537-45. doi: 10.1002/hep.510270231.

引用本文的文献

1
A metabolomic perspective of griseofulvin-induced liver injury in mice.灰黄霉素诱导小鼠肝损伤的代谢组学研究视角
Biochem Pharmacol. 2015 Dec 1;98(3):493-501. doi: 10.1016/j.bcp.2015.09.002. Epub 2015 Sep 5.
2
Autophagy and apoptosis in liver injury.肝脏损伤中的自噬与凋亡
Cell Cycle. 2015;14(11):1631-42. doi: 10.1080/15384101.2015.1038685.
3
Role of p62/SQSTM1 in liver physiology and pathogenesis.p62/SQSTM1 在肝脏生理和发病机制中的作用。
Exp Biol Med (Maywood). 2013 May;238(5):525-38. doi: 10.1177/1535370213489446.
4
Bile acid-induced Mallory body formation in drug-primed mouse liver.胆汁酸诱导药物预处理小鼠肝脏中马洛里小体的形成。
Am J Pathol. 2002 Dec;161(6):2019-26. doi: 10.1016/S0002-9440(10)64480-X.
5
Protoporphyrin-induced cholestasis in the isolated in situ perfused rat liver.原卟啉诱导的原位灌注大鼠肝脏胆汁淤积
J Clin Invest. 1981 Feb;67(2):385-94. doi: 10.1172/JCI110046.
6
Drug-induced cholestasis.药物性胆汁淤积
Med Toxicol. 1987 Mar-Apr;2(2):112-60. doi: 10.1007/BF03260010.