期刊文献+

胆道损伤愈合过程中cIAP-1及caspase3的表达及其意义 被引量:1

The expression and significance of caspase3 and cIAP-1 in the wound healing process of bile duct
下载PDF
导出
摘要 目的观察凋亡调控蛋白cIAP1及其下游凋亡因子caspase3在胆道良性狭窄形成过程中的表达和定位情况,并探讨其意义。方法建立胆管损伤后愈合犬模型,分别利用原位杂交检测技术及免疫组织化学过氧化酶标记的链霉卵白素(Streptavidin Peroxidase Method,SP)法对犬胆道损伤愈合不同时期的组织中cIAP1及caspase3的表达和定位情况进行分析。结果 cIAP1于各时间点均显著性表达(P<0.05),定位于间质细胞,以成纤维细胞为甚;各组间差异无统计学意义(P>0.05)。Caspase3表达明显弱于对照组(P<0.05),腺上皮表达相对较强,各期之间差异无统计学意义(P>0.05)。cIAP-1mRNA与caspase3蛋白表达呈负相关(r=-0.97,P<0.05)。结论抗凋亡基因cIAP-1通过抑制其下游凋亡因子caspase3可能在胆道损伤后的瘢痕愈合转归中发挥重要作用。 Objective To observe the expression and localization of the apoptosis regulation protein clAP1 and its downstream factor caspase3 in the course of the formation of benign biliary stricture and to explore its significance. Methods After establishment of canine model for healing after bile duct injury, expression and localization of cIAP1 and caspase3 in biliary tissue at different stages of healing were analyzed by using in situ hybridization technique and immunohistochemical peroxidase labeled avidin-streptavidin (Streptavidin Peroxidase Method, SP) method, respectively. Results cIAP1 was significantly expressed at all time points ( P 〈 0.05 ). The expression was located in the interstitial cells, especially in fibroblasts. There was no significant difference among the healing stages ( P 〉 0.05 ). The expression of caspase3 in the experimental group was significantly less than that in the control group ( P 〈0. 05 ). The expression in epithelial cells was relatively stronger. There was no significant difference among the healing stages ( P 〉 0.05 ). There was a negative correlation between cIAP-1 mRNA and caspase3 protein ( r = -0. 97,P 〈0. 05 ). Conclusion The inhibition of caspase3 by cIAP-1 may play an important role in sear-less healing after bile duct injury.
出处 《实用医院临床杂志》 2016年第5期87-90,共4页 Practical Journal of Clinical Medicine
关键词 胆道 原位杂交 免疫组化 凋亡 cIAP1 CASPASE3 Biliary In situ hybridization Immunohistochemistry Apoptosis cIAP1 Caspase3
  • 相关文献

参考文献4

二级参考文献135

  • 1[46]Sun AQ,Arrese MA,Zeng L,Swaby I,Zhou MM,Suchy FJ.The rat liver Na(+)/bile acid cotransporter.Importance of the cytoplasmic tail to function and plasma membrane targeting.J Biol Chem 2001; 276:6825-6833
  • 2[47]Reymann A,Braun W,Drobik C,Woermann C.Stimulation of bile acid active transport related to increased mucosal cyclic AMP content in rat ileum in vitro.Biochim Biophys Acta 1989;1011:158-164
  • 3[48]Alpini G,Glaser S,Chowdhury U,Francis H,Kanno N,Phinizy JL,Eisel W,LeSage G.cAMP-dependent translocation of the apical bile acid transporter (ABAT) to the cholangiocyte apical membrane regulates ductal absorption of conjugated bile acids.Hepatology 1999; 30:A1029
  • 4[49]Alpini G,Glaser S,Alvaro D,Ueno Y,Marzioni M,Francis H,Baiocchi L,Stati T,Barbaro B,Phinizy JL,Mauldin J,Lesage G.Bile acid depletion and repletion regulate cholangiocyte growth and secretion by a phosphatidylinositol 3-kinase-dependent pathway in rats.Gastroenterology 2002; 123:1226-1237
  • 5[50]Chen F,Ma L,Sartor RB,Li F,Xiong H,Sun AQ,Shneider B.Inflammatory-mediated repression of the rat ileal sodiumdependent bile acid transporter by c-fos nuclear translocation.Gastroenterology 2002; 123:2005-2016
  • 6[51]Skach WR.Defects in processing and trafficking of the cystic fibrosis transmembrane conductance regulator.Kidney Int 2000; 57:825-831
  • 7[52]Hatakeyama S,Nakayama KI.Ubiquitylation as a quality control system for intracellular proteins.J Biochem (Tokyo) 2003;134:1-8
  • 8[53]Schwartz DC,Hochstrasser M.A superfamily of protein tags:ubiquitin,SUMO and related modifiers.Trends Biochem Sci 2003; 28:321-328
  • 9[54]Alpini G,Glaser S,Robertson W,Rodgers RE,Phinizy JL,Lasater J,LeSage GD.Large but not small intrahepatic bile ducts are involved in secretin-regulated ductal bile secretion.Am J Physiol 1997; 272:G1064-1074
  • 10[55]Alpini G,Roberts S,Kuntz SM,Ueno Y,Gubba S,Podila PV,LeSage G,LaRusso NF.Morphological,molecular,and functional heterogeneity of cholangiocytes from normal rat liver.Gastroenterology 1996; 110:1636-1643

共引文献72

同被引文献2

引证文献1

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