【摘要】 目的 探討凋亡抑制蛋白Livin與凋亡蛋白Caspase-3在結(jié)直腸腺瘤-癌序列中的表達(dá)變化及其相關(guān)性?！》椒ā?006年7月—2009年12月，采用免疫組織化學(xué)染色鏈霉菌抗生物素蛋白-過(guò)氧化物酶鏈接法streptavidin-peroxidese，SP）法檢測(cè)18例正常黏膜、84例結(jié)直腸腺瘤、72例結(jié)直腸癌中Livin及Caspase-3的表達(dá)情況?！〗Y(jié)果 結(jié)直腸腺瘤組織中Livin蛋白的陽(yáng)性表達(dá)率明顯高于正常黏膜組織（Plt;0.05），而低于腺癌組（Plt;0.05）；腺瘤組內(nèi)絨毛狀腺瘤與管狀腺瘤相比較，Livin蛋白表達(dá)率差異有統(tǒng)計(jì)學(xué)意義（Plt;0.05）。結(jié)直腸腺瘤組織中Caspase-3的陽(yáng)性表達(dá)率明顯高于正常黏膜組織（Plt;0.05）；而腺瘤組織與癌組織之間Caspase-3陽(yáng)性表達(dá)率差異（Plt;0.05）；腺瘤組內(nèi)絨毛狀腺瘤與管狀腺瘤相比較，Caspase-3蛋白陽(yáng)性表達(dá)率差異無(wú)統(tǒng)計(jì)學(xué)意義（Pgt;0.05）。Livin表達(dá)與Caspase-3表達(dá)呈負(fù)相關(guān)（Plt;0.05）?！〗Y(jié)論 凋亡抑制蛋白Livin參與了大腸腫瘤的發(fā)生，且在大腸腺瘤-腺癌階段起到了重要作用；凋亡抑制蛋白Livin與Caspase-3表達(dá)呈負(fù)相關(guān)，抑制Caspase-3蛋白的活性可能是Livin促進(jìn)結(jié)腸癌發(fā)生的途徑之一?！続bstract】 Objective To investigate the expression of Livin and Caspase-3 among colorectal adenoma-carcinoma sequence, and to identify the relationship between Livin and Caspase-3 expression in colorectal adenoma-carcinoma sequence. Methods Formalin-fixed paraffin embedded colorectal tissues from 174 patients, including 84 adenomas, 72 carcinomas, and 18 normal mucosa, were examined for expression of Livin and Caspase-3 by streptavidin-peroxidase (SP) immunohistochemistry between July 2006 and December 2009. Results The positive rates of Livin protein expression in colorectal adenoma was significantly higher than that in normal mucosa (Plt;0.05), but lower than that in adenocarcinoma (Plt;0.05); the expression of Livin in tubular adenoma was significantly higher than that in villous adenoma (Plt;0.05). The positive rates of Caspase-3 protein expression in colorectal adenoma were significantly higher than that in normal mucosa and carcinoma (Plt;0.05), and the difference in positive rate of Caspase-3 expression was not significant between the villous adenoma and tubular adenoma (Pgt;0.05). Livin expression had negative correlation with the Caspase-3 expression (Pgt;0.05). Conclusion The difference in expression of Livin between adenoma and adenocarcinoma indicates the potential value of it in carcinogenesis of colorectal cancer, which suggestes that suppressing Caspase-3 protein activity is one of the channels by which livin promotes colorectal carcinogenesis.