|本期目录/Table of Contents|

[1]李萌乾,王青松,郭正隆,等.诱导型狨猴肝纤维化模型的建立 [J].天津医科大学学报,2014,20(06):433-436.
　LI Meng-qian,WANG Qing-song,GUO Zheng-long,et al. Establishment of drug-induced common marmoset model for hepatic fibrosis[J].Journal of Tianjin Medical University,2014,20(06):433-436.
点击复制

诱导型狨猴肝纤维化模型的建立


 
(PDF)
分享到：

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
20卷
期数:
2014年06期
页码:
433-436
栏目:
基础医学
出版日期:
2014-11-20

文章信息/Info

Title:
 Establishment of drug-induced common marmoset model for hepatic fibrosis
文章编号:
1006-8147（2014）06-0433-04
作者:
李萌乾; 王青松; 郭正隆; 尹海芳
（天津医科大学基础医学研究中心，天津医科大学细胞生物学系，天津 300070）
Author(s):
LI Meng-qian; WANG Qing-song; GUO Zheng-long; YIN Hai-fang
(Research Centre of Basic Medical Science，Department of Cell Biology, Tianjin Medical University, Tianjin 300070, China)
关键词:
肝纤维化; 普通狨猴; 二乙基亚硝胺; 肝切除
Keywords:
hepatic fibrosis;  common marmoset;  diethylnirtosamine; hepatectomy
分类号:
R575.2
DOI:
-
文献标志码:
A
摘要:
目的：建立诱导型狨猴肝纤维化模型。方法：手术切除普通狨猴部分肝脏，通过腹腔注射二乙基亚硝胺（DENA-2.5 mg/kg)，并利用体质量和肝功能检测、病理分析、免疫组化，胶原染色和B超小动物活体成像等手段进行监测。结果：手术切除肝脏促使狨猴肝脏再生，并伴随肥大和炎症反应；DENA药物诱导会引发与人类类似的肝脏炎症，肝脏胶原聚集和血管增生，最终导致狨猴肝脏纤维化。结论：手术切肝联合DENA化学诱导可以成功获得狨猴肝纤维化模型。
Abstract:
Objective: To establish the drug-induced common marmoset model for hepatic fibrosis. Methods: Hepatectomy and intraperitoneal injection of DENA at the dose of 2.5 mg/kg was used and various assays were performed to monitor the bodyweight, liver function, pathology, and collagen in common marmosets. Furthermore, non-invasive imaging systems were applied i.e. B ultrasound and live animal imaging. Results: The generation of newborn liver and inflammation was accelerated by hepatectomy. DENA was effective in inducing hepatitis, vascular proliferation, accumulation of collagen and fibrosis as observed in clinic. Conclusion: Successfully establishes the common marmoset model for hepatic fibrosis with the combination of hepatectomyand DENA.

参考文献/References:

[1]Smyth R, Munday M R, York M J, et al. Comprehensive characterization of serum clinical chemistry parameters and the identification of urinary superoxide dismutase in a Carbon tetrachloride-induced model of hepatic fibrosis in the female Hanover Wistar rat[J]. Int J ExpPathol, 2007,88(5):361

[2]Zhao J, Zhou G, Li M, et al. A novel non-alcoholic steatohepatitis animal model featured with insulin resistance, hepatic inflammation and fibrosis[J]. Scand J Gastroenterol, 2010,45(11):1360

[3]Yermakoff J K, Fuller G C, Rodil J V. An experimental model of hepatic fibrosis induced by the administration of dibutyltindichloride[J]. ToxicolApplPharmacol, 1979,49(1):31

[4]Kishi N, Sato K, Sasaki E, et al. Common marmoset as a new model animal for neuroscience research and genome editing technology[J]. Dev Growth Differ, 2014,56(1):53

[5]Ludlage E, Mansfield K. Clinical care and diseases of the common marmoset (Callithrixjacchus)[J]. Comp Med, 2003,53(4):369

[6]Kovalszky I, Szeberenyi S, Zalatnai A, et al. Modification of DENA-induced hepatocarcinogenesis by CCl4 cirrhosis. Comparison of the marker enzyme patterns[J]. Carcinogenesis, 1992,13(5):773

[7]Aboul-Ela L M, Shaaban S.A lab-clinical study of reinforced acrylic resin dentures.Composite dentures. Part II[J]. Alex Dent J, 1977,2(2):73

[8]Dufour D R, Kost G J. Critical values launch interpretive Lab medicine and clinical pathology. Interview by CarrenBersch and Kristin N. Hale[J]. MLO Med Lab Obs, 2009,41(3):18

[9]Villiers E. Applications of clinical pathology: from the practice Lab to the research bench[J]. J Small AnimPract, 2007,48(10):543

[10]Gäbele E, Dostert K, Dorn C, et al. A new model of interactive effects of alcohol and high-fat diet on hepatic fibrosis[J]. Alcohol ClinExp Res, 2011,35(7):1361

[11]Goo M J, Ki M R, Lee H R, et al. Helicobacter pylori promotes hepatic fibrosis in the animal model[J]. Lab Invest, 2009,89(11):1291

[12]Chae H B, Jang L C, Park S M, et al. An experimental model of hepatic fibrosis induced by alcohol and CCl4: can the lipopolysaccharide prevent liver injury induced by alcohol and CCl4?[J]. TaehanKanHakhoe Chi, 2002,8(2):173

[13]Müller V, Brummer D, Erhardt W, et al. Arterialisation of the portal vein as a model for the induction of hepatic fibrosis: description of microsurgical models in the rat[J]. TransplInt, 2005,17(12):822

[14]Gonnert F A, Kunisch E, Gajda M, et al. Hepatic fibrosis in a long-term murine model of sepsis[J]. Shock, 2012,37(4):399

[15]Wang B E, Jia J D, Zhang W S. Progress in non-invasive diagnostic model of hepatic fibrosis[J]. ZhongguoZhong Xi Yi Jie He ZaZhi, 2006,26(1):5

[16]Jung S A, Chung Y H, Park N H, et al. Experimental model of hepatic fibrosis following repeated periportal necrosis induced by allylalcohol[J]. Scand J Gastroenterol, 2000,35(9):969

相似文献/References:

[1]刘文东,李英娴,娄婷婷,等.青蒿琥酯对肝纤维化大鼠肝组织基质金属蛋白酶表达的影响[J].天津医科大学学报,2013,19(05):362.
[2]徐亚洁,张晓燕,马淑晶,等.神经酰胺对肝纤维化治疗作用的初步研究[J].天津医科大学学报,2014,20(04):260.
　XU Ya-jie,ZHANG Xiao-yan,MA Shu-jing,et al.Effects of ceramide on hepatic fibrosis[J].Journal of Tianjin Medical University,2014,20(06):260.
[3]张晓燕,马淑晶,徐亚洁,等.青蒿琥酯对人源肝星状细胞LX-2增殖、胶原产生以及KLF6表达的影响[J].天津医科大学学报,2014,20(04):257.
　ZHANG Xiao-yan,MA Shu-jing,XU Ya-jie,et al.Effects of artesunate on cell proliferation，collagen generated and KLF6 expression in hepatic stellate cells[J].Journal of Tianjin Medical University,2014,20(06):257.
[4]刘 悦,李杉杉,唐诗慧,等.蒿鳖养阴软坚方通过激活Nrf2/NQO1信号通路抑制肝纤维化发生[J].天津医科大学学报,2018,24(01):19.
　LIU Yue,LI Shan-shan,TANG Shi-hui,et al.Effects of HaobieYangyinRuanjian on inhibition of hepatic fibroesis through upregulated Nrf2/NQO1 pathway[J].Journal of Tianjin Medical University,2018,24(06):19.
[5]卢娜,方步武.蒿鳖养阴软坚方对刀豆球蛋白A诱导的肝纤维化Nrf2/HO-1信号通路影响[J].天津医科大学学报,2018,24(02):112.
　LU Na,FANG Bu-wu.Effect of Haobie yangyin ruanjian prescription on Nrf2/HO-1 signaling pathway in ConA-induced hepatic fibrosis[J].Journal of Tianjin Medical University,2018,24(06):112.
[6]张丽,方步武.虎杖苷抑制肝星状细胞增殖活化的作用和机制研究[J].天津医科大学学报,2020,26(04):309.
　ZHANG Li,FANG Bu-wu.Inhibitory effects and mechanism of Polydatin on the proliferation and activation of hepatic stellate cell[J].Journal of Tianjin Medical University,2020,26(06):309.
[7]靳悦,汪河,李明威,等.CD24 通过调节肝内Ly6Clo 巨噬细胞亚群中PDGF-B 的 分泌抑制肝纤维化进程[J].天津医科大学学报,2022,28(03):260.
　JIN Yue,WANG He,LI Ming-wei,et al.CD24 inhibits the liver fibrosis process by regulating the secretion of PDGF -B in hepatic Ly6Clo macrophage subset[J].Journal of Tianjin Medical University,2022,28(06):260.
[8]刘志杰综述,詹江华审校.肝巨噬细胞在胆道闭锁肝纤维化中的作用[J].天津医科大学学报,2023,29(04):453.
[9]翁飞鸿,周一平,伊思敏,等.肝纤维化的病理学发生机制及诊疗研究进展[J].天津医科大学学报,2023,29(05):559.
[10]马立业,程欣欣,徐哲龙.p67phox在肝纤维化中的作用及其机制[J].天津医科大学学报,2024,30(06):514.[doi:10.20135/j.issn.1006-8147.2024.06.0514]
　MA Liye,CHENG Xinxin,XU Zhelong.The role of p67phox in hepatic fibrosis and the underlying mechanism[J].Journal of Tianjin Medical University,2024,30(06):514.[doi:10.20135/j.issn.1006-8147.2024.06.0514]

备注/Memo

备注/Memo:

基金项目 国家 973 重大科学研究计划资助项目（2012CBA01305）

作者简介 李萌乾（1988-），男，硕士在读，研究方向：肝癌肝损伤模型；通信作者：尹海芳，E-mail：haifangyin@tmu.edu.cn。

更新日期/Last Update: 2014-11-21