银杏叶对黄曲霉毒素B1诱发大鼠肝癌IGF-ⅡmRNA及蛋白表达影响的观察

Effects of Ginkogo biloba on the expression of IGF-ⅡmRNA and protein during hepatocarcinogenesis aflatoxin B1-induced in wistar rats

目的:动态观察银杏叶提取物(EGb761)在抑制黄曲霉毒素B1(AFB1)诱发大鼠肝癌(HCC)过程中对肝组织相关基因IGF-ⅡmRNA及蛋白表达水平的影响,从分子生物学水平揭示银杏叶抗癌的机制及其效果。方法:将70只4周龄Wistar雄性大鼠随机分为AFB1组(25只)、AFB1+EGb761组(25只)及对照组(20只)。在诱发大鼠HCC过程中,分别于第13周、33周及53周对大鼠进行肝组织活检;实验至第73周处死全部动物取肝组织。利用实时荧光定量PCR和蛋白质印迹法动态检测肝组织中IGF-ⅡmRNA及相应蛋白的表达情况。结果:AFB1组原发性HCC发生率为58.8%(10/17);AFB1+EGb761组发生率为29.4%(5/17);对照组为0(0/16)。AFB1+EGb761组HCC发生率显著低于AFB1组(P<0.05)。AFB1+EGb761组肝组织IGF-2mRNA及相应蛋白表达水平在第53周及73周较AFB1组均显著下降,差异有统计学意义,P<0.05。结论:银杏叶提取物(EGb761)具有抑制AFB1致大鼠HCC的作用。其机制可能与调控肝细胞增殖基因IGF-ⅡmRNA及蛋白表达水平有关。

OBJECTIVE： To investigate the effects of Ginkgo giloba extract （extraet 761 from Ginkgo giloba, EGb761） on the expression of IGF-Ⅱ mRNA and protein during hepatocarcinogenesis induced by aflatoxin B1 （AFB1） in wistar rats. METHODS： Seventy Wistar rats were randomly divided into 5 groups： AFB1 group （25）, AFB1 ＋ EGb761 group （25） and ControI group （20）. During hepatoearcinogenesis liver biopsies were performed on all animals at 13th-, 33rd-, and 53rd-week of the experiment respectively. Animals were sacrificed at the 73rd-week and liver tissues were col- lected. The expression of IGF-Ⅱ mRNA of hepatocyte were detected by Real-time PCR technology and the relative protein expression in liver tissue were observed by Western Blotting array. RESULTS： The rate of primary hepatocellular carcino- ma （PHC） in AFB1 group was 58.8%0（10/17） ; AFBl＋EGb761 group was 29.4~/00（5/17） ; Control group was 0（0/16）. The rate of PHC in Ginkogo biloba group is significantly lower than that in AFB1 group （P^0.05）. The expression of IGF- ]l mRNA and the relative protein expression in Ginkogo biloba group were both significantly lower than that in AFB1 group at 53rd-and 73rd-week of the experiment （P〈0.05）. CONCLUSIONS： The Ginkogo biloba can effectively inhibite the occurrence of primary hepatocellular carcinoma induced by AFB1. The mechanism of treatment may be relative to reg- ulate expression of IGF-Ⅱ mRNA and the protein.