期刊文献+

β-arrestin 1在小鼠非酒精性脂肪性肝病至肝癌自然病程中的作用 被引量:1

Role of β-arrestin 1 in the course of non-alcoholic fatty liver disease progressing to hepatocellular carcinoma
原文传递
导出
摘要 目的探讨β-arrestin 1在小鼠非酒精性脂肪性肝病(NAFLD)至肝癌自然病程中的变化和作用。方法健康雄性C57BL/6小鼠80只,按随机数字表法随机分为素食组和高脂饮食组,每组各40只,分别给予素食(脂肪含量占总热量13%)和高脂饮食(脂肪含量占总热量58%),两组9、24周末时分别各处死8只小鼠,48周末时处死剩余小鼠。观察两组小鼠的肝癌发生率。Western blot法检测小鼠肝组织β-arrestin 1蛋白表达,Taq Man实时荧光定量RT-PCR检测其β-arrestin 1的m RNA水平。两组小鼠肝癌发生率的比较采用Fisher确切概率法,β-arrestin 1蛋白及其m RNA水平比较采用t检验。高脂饮食组β-arrestin 1蛋白和m RNA水平与高脂饮食时间的关系分析采用Spearman相关分析。结果高脂饮食组小鼠肝癌的发生率为18%(4/22),明显高于素食组的0(0/23)(P=0.034)。高脂饮食组小鼠9周时肝组织β-arrestin 1蛋白表达水平为2.4±0.5,明显高于素食组的1.5±0.4(t=2.779,P<0.05)。高脂饮食组小鼠9、24、48周肝组织β-arrestin 1的m RNA水平分别为4.1±0.8、7.8±2.1、12.5±1.2,明显高于同期素食组的2.6±0.7、3.6±0.6、6.9±1.2(t=4.029,5.522,9.487;P<0.05)。高脂饮食组小鼠48周时肝癌组织的β-arrestin 1蛋白和m RNA水平为4.6±0.5、22.0±3.2,明显高于同期肝组织的1.6±0.4、12.5±1.2(t=9.600,7.837;P<0.05)。高脂饮食组的β-arrestin 1蛋白和m RNA水平与高脂饮食时间呈正相关(r=0.949,0.922;P<0.05)。结论小鼠高脂饮食易发生NAFLD,且发生肝癌的几率明显升高。β-arrestin 1在此过程中可能起促进作用。 ObjectiveTo investigate the changes and role of β-arrestin 1 in the course of non-alcoholic fatty liver disease (NAFLD) progressing to hepatocellular carcinoma (HCC). MethodsEighty healthy male C57BL/6 mice were randomized into the vegetarian diet group and the high fat diet group according to the random number table with 40 mice in each group. Mice in the vegetarian diet group were fed with vegetarian diet (13% calories in fat) and mice in the high fat diet group were fed with high fat diet (58% calories in fat). Eight mice in each group were decapitated at the end of 9 and 24 weeks. The rest mice in each group were decapitated at the end of 48 weeks. The incidence of HCC of two groups was observed. The expression of proteinβ-arrestin 1 in the liver tissues of mice was detected by Western blot and the mRNA level was examined using TaqMan real time fluorescence quantitative RT-PCR. The incidence of HCC in two groups was compared using Fisher's exact test, and the protein β-arrestin 1 expression and mRNA level of two groups were compared usingt test. Spearman correlation analysis was used to evaluate the relationship between protein β-arrestin 1 expression, mRNA level and the feeding duration of high fat diet in high fat diet group.ResultsThe incidence of HCC in the high fat diet group was 18% (4/22), which was significantly higher than 0 (0/23) in the vegetarian diet group (P=0.034). The expression level of protein β-arrestin 1 in liver tissues of mice in the high fat diet group was 2.4±0.5 in the 9th week, which was significantly higher than 1.5±0.4 in the vegetarian diet group (t=2.779,P<0.05). The β-arrestin 1 mRNA level in liver tissues of mice in the high fat diet group in the 9th, 24th and 48th week were 4.1±0.8, 7.8±2.1 and 12.5±1.2 respectively, which were all significantly higher than 2.6±0.7, 3.6±0.6 and 6.9±1.2 in the vegetarian diet group (t=4.029, 5.522, 9.487;P<0.05) . The protein β-arrestin 1 and mRNA level in HCC tissues of mice in the high fat diet group in the 48th week were 4.6±
出处 《中华肝脏外科手术学电子杂志》 CAS 2015年第6期372-376,共5页 Chinese Journal of Hepatic Surgery(Electronic Edition)
基金 广东省科技计划项目(2008B030301038 2012B061700072)
关键词 脂肪肝 肝细胞 Β-ARRESTIN 小鼠 Fatty liver Carcinoma,hepatocellular β-arrestin Mice
  • 相关文献

参考文献2

二级参考文献51

  • 1Nobuhisa Akamatsu,Yasuhiko Sugawara,Norihiro Kokudo.Living-donor vs deceased-donor liver transplantation for patients with hepatocellular carcinoma[J].World Journal of Hepatology,2014,6(9):626-631. 被引量:14
  • 2Torre LA, Bray F, Siegel RL, Ferlay J, Lortet-Tieulent J, Jemal A.Global cancer statistics, 2012. CA Cancer J Clin 2015; 65: 87-108#[PMID: 25651787 DOI: 10.3322/caac.21262]. 被引量:1
  • 3Scaggiante B, Kazemi M, Pozzato G, Dapas B, Farra R, Grassi M,Zanconati F, Grassi G. Novel hepatocellular carcinoma moleculeswith prognostic and therapeutic potentials. World J Gastroenterol2014; 20: 1268-1288 [PMID: 24574801 DOI: 10.3748/wjg.v20.i5.1268]. 被引量:1
  • 4Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Globalcancer statistics. CA Cancer J Clin 2011; 61: 69-90 [PMID:21296855 DOI: 10.3322/caac.20107]. 被引量:1
  • 5Llovet JM, Bruix J. Systematic review of randomized trialsfor unresectable hepatocellular carcinoma: Chemoembolizationimproves survival. Hepatology 2003; 37: 429-442 [PMID:12540794 DOI: 10.1053/jhep.2003.50047]. 被引量:1
  • 6Chan SL, Yeo W. Targeted therapy of hepatocellular carcinoma:present and future. J Gastroenterol Hepatol 2012; 27: 862-872[PMID: 22369685 DOI: 10.1111/j.1440-1746.2012.07096.x]. 被引量:1
  • 7Chi KN, Zoubeidi A, Gleave ME. Custirsen (OGX-011): a secondgenerationantisense inhibitor of clusterin for the treatment ofcancer. Expert Opin Investig Drugs 2008; 17: 1955-1962 [PMID:19012510 DOI: 10.1517/13543780802528609]. 被引量:1
  • 8Zielinski R, Chi KN. Custirsen (OGX-011): a second-generationantisense inhibitor of clusterin in development for the treatmentof prostate cancer. Future Oncol 2012; 8: 1239-1251 [PMID:23130925 DOI: 10.2217/fon.12.129]. 被引量:1
  • 9Wong P, Borst DE, Farber D, Danciger JS, Tenniswood M,Chader GJ, van Veen T. Increased TRPM-2/clusterin mRNAlevels during the time of retinal degeneration in mouse models ofretinitis pigmentosa. Biochem Cell Biol 1994; 72: 439-446 [PMID:7605616]. 被引量:1
  • 10Zhang Q, Zhou W, Kundu S, Jang TL, Yang X, Pins M, SmithN, Jovanovic B, Xin D, Liang L, Guo Y, Lee C. The leadersequence triggers and enhances several functions of clusterin andis instrumental in the progression of human prostate cancer in vivoand in vitro. BJU Int 2006; 98: 452-460 [PMID: 16879694 DOI:10.1111/j.1464-410X.2006.06263.x]. 被引量:1

共引文献28

同被引文献24

引证文献1

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部