摘要
目的 观察大鼠诱癌过程中c mycmRNA的动态演变规律以及乌司他丁对其表达的影响。方法 将SD大鼠 12 0只分为正常组、诱癌组和干预组。利用诱癌剂 3 甲基 2 甲氨基偶氮苯 (DAB)喂养SD大鼠来制作肝癌模型。各组于肝癌开始造模后 2、4、6、8、10、12、14、16、18、2 0、2 2、2 4周分别活杀取肝叶标本 ,采用逆转录 聚合酶链反应 (RT PCR )技术检测c mycmRNA的表达。结果 c myc基因在正常大鼠肝组织内呈阳性表达 ,从肝脏染毒开始即升高。在癌变期 (14~2 4周 ) ,c mycmRNA的表达量亦逐渐增高 (5 .69± 1.3 5 )~ (8.16± 2 .18)。乌司他丁的干预不能抑制c mycmRNA的表达量的升高 ,但能推迟其表达量的升高的时间。 结论 c myc作为一种致癌基因可能是肝癌的启动基因和维持基因 ,其表达量也是一种肝细胞癌的恶性程度和进展期的标志基因。乌司他丁在一定程度上可抑制肝损伤和肝细胞癌的发生 ,但不能抑制c myc基因的表达。
Objective To study the dynamic changes of c-myc mRNA and the effects of urinary trypsin inhibitor (UTI) during the hepatocarcinogenesis in rats.Methods 120 SD rats were divided into normal group,induced-cancer group and interfered group.3'-methyl-dimethylaminoazobenzene (DAB) was used to feed SD rats to construct hepatocellular carcinoma model.Liver samples were collected in each group at the 2nd,4th,6th,8th,10th,12th,14th,16th,20th,24th week respectively.The expression of c-myc mRNA was detected by RT-PCR.Results The expression of c-myc mRNA was positive in normal rat liver tissue and began to increase after liver exposed to DAB.During hepatocarcinogenesis (14 to 24 weeks),the expression of c-myc mRNA was gradually increased from 5.69±1.35 to 8.16±2.18.UTI couldn't inhibit the increased expression of c-myc mRNA,but could delay the up-regulation of the c-myc mRNA.Conclusion C-myc may be a promotor gene and phenocopy gene of hepatocellular carcinoma,and its expression can indicate the hepatocarcinogenesis process.UTI can inhibit the hepatic damage and the hepatocarcinogenesis to some extent,but can't suppress the expression of c-myc gene.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2004年第3期298-300,共3页
Chinese Journal of Experimental Surgery
基金
广东省自然科学基金资助项目 (2 0 0 1 0 1 0 593
2 0 0 2 0 2 0 0 97)