期刊文献+

老鼠簕对四氯化碳致肝纤维化大鼠Toll样受体4表达的影响 被引量:5

Effect of Acanthus ilicifolius Linnseus on Toll-like receptor 4 expressions of hepatic fibrosis induced by carbon tetrachloride in rats
下载PDF
导出
摘要 目的研究老鼠簕对四氯化碳(CCl4)诱导的肝纤维化大鼠肝组织Toll样受体4(TLR4)表达的影响。方法 Wistar大鼠随机分为空白对照组、模型对照组、秋水仙碱组、老鼠簕乙醇提取物低剂量组和老鼠簕乙醇提取物高剂量组。除空白对照组外,其余4组用CCl4制备大鼠肝纤维化模型。秋水仙碱组、老鼠簕乙醇提取物低剂量组和老鼠簕乙醇提取物高剂量组分别于4周后给予相应的药物,空白对照组和模型对照组给予等容量的生理盐水,每日1次。8周后处死大鼠。逆转录-聚合酶链反应(RT-PCR)检测肝组织中TLR4 mRNA的表达。结果 RT-PCR结果显示,与空白对照组相比,模型对照组TLR4 mRNA表达增强(P<0.01);老鼠簕乙醇提取物干预组(1.0、2.0 g.kg-1)较模型对照组TLR4 mRNA表达减弱(P<0.05)。结论老鼠簕能够抑制肝纤维化大鼠肝组织TLR4的表达。 Objective To explore the effect of Acanthus ilicifolius Linnseus on Toll-like receptor 4(TLR4) expressions of the hepatic fibrosis induced by carbon tetrachloride(CCl4) in rats.Methods Wistar rats were randomly divided into normal control group,model control group,colchicine group,low dosage group and high dosage group of ethanol extract of Acanthus ilicifolius(EEA).Except the normal control group,the other four groups were injected CCl4 to establish hepatic fibrosis model.Four weeks later,the colchicine group,the EEA low dosage group and the EEA high dosage group were treated with colchicine and EEA respectively,the normal control group and the model control group were treated with normal saline.All rats were sacrificed administration for eight weeks.The TLR4 mRNA expressions were detected by reverse transcription polymerase chain reaction.Results Compared with normal control group,the levels of TLR4 expression in model control group were elevated(P0.01);the levels of TLR4 expression in the EEA-treated(1.0,2.0 g·kg-1) groups were decreased compare with model control group(P0.05).Conclusion Acanthus ilicifolius Linnseus can inhibit TLR4 expressions in liver fibrotic rats.
出处 《新乡医学院学报》 CAS 2012年第2期93-95,共3页 Journal of Xinxiang Medical University
关键词 肝纤维化 老鼠簕 TOLL样受体4 hepatic fibrosis Acanthus ilicifolius Linnseus Toll-like receptor 4
  • 相关文献

参考文献9

二级参考文献66

共引文献18

同被引文献73

  • 1王丽娜,刘成海,陈园,陶艳艳,周滔,陈高峰.一种改良的二甲基亚硝胺肝纤维化模型诱导方法及其病理特点[J].中国实验动物学报,2007,15(2):90-94. 被引量:17
  • 2Gasparini C, Feldmann M. NF-KB as a target for modulating in- flammatory responses [ J ]. Curt Pharm Des, 2012,18 ( 35 ) : 5735- 5745. 被引量:1
  • 3Lewander A, Gao J, Adell G,et al. Expression of NF-κB p65 phos- phorylated at serine-536 in rectal cancer with or without preopera- tive radiotherapy [ J ]. Radiol Oncol,2011,45 (4) :279-284. 被引量:1
  • 4Bartlett N W, Slater L, Glanville N, et al. Defining critical roles for NF-KB p65 and type I interferon in innate immunity to rhinovirus[J]. EMBO Mol Med ,2012,4 ( 12 ) : 1244-1260. 被引量:1
  • 5Kiessling M K, Linke B, Brechmann M, et al. Inhibition of NF-KB induces a switch from CD95L-dependent to CD95L-independent and JNK-mediated apoptosis in T ceils [ J ]. FEBS Lett, 2010,584 (22) :4679-4688. 被引量:1
  • 6Sunami Y, Leithauser F, Gul S, et al. Hepatic activation of IKK/ NF-κB signaling induces liver fibrosis via maerophage-mediated chronic inflammation [ J ]. Hepatology, 2012,56 ( 3 ) : 1117-1128. 被引量:1
  • 7Sen R, Baltimore D. Inducibility of kappa immunoglobulin enhan- cer-binding protein NF-kappa B by a posttranslational mechanism [ J ]. Cell, 1986,47 ( 6 ) :921-928. 被引量:1
  • 8Zhang N N,Sun Q S,Chen Z,et al. Homeostatic regulatory role of Pokemon in NF-KB signaling:stimulating both p65 and IκBα ex- pression in human hepatocellular carcinoma cells [ J ]. Mol Cell Biochem ,2013,372 ( 1/2 ) :57-64. 被引量:1
  • 9Stollenwerk M M, Lasson A, Andersson R. Active site-inactivated factor VIIa inhibits nuclear factor kappa B activation in intestinal ischemia and reperfusion [ J ]. J Surg Res, 2012, 178 ( 2 ) : 692- 699. 被引量:1
  • 10Williams V, Brichler S, Khan E, et al. Large hepatitis delta anti- gen activates STAT-3 and NF-κB via oxidative stress[ J ]. J Viral Hepat,2012,19(10 ) :744-753. 被引量:1

引证文献5

二级引证文献28

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