绞股蓝总甙对金地鼠颊囊白斑癌变过程中端粒酶活性化学预防作用研究  

Altered telomerase activity during chemoprevention of experimental hamster cheek pouch carcinogenesis by Gynostempa Pentaphyllum Mak.

作　　者：娄佳宁[1] 周曾同[2] 

机构地区：[1]上海交通大学附属第一人民医院口腔科,上海200080 [2]上海交通大学医学院附属第九人民医院口腔黏膜病科

出　　处：《临床口腔医学杂志》2008年第4期234-237,共4页Journal of Clinical Stomatology

基　　金：国家自然科学基金资助(39870928)

摘　　要：目的:探讨中药绞股蓝(Gynostema Pentaphyllum Mak,GP)对实验性口腔白斑癌变过程的干预作用及其对端粒酶活性影响,探索GP防癌的可能药理机制。方法:以Salley法建立金地鼠颊囊癌变模型,GP进行体内干预,160只实验动物分4组:空白对照组(A组);模型对照组(B组);先、后服用GP组(C组、D组)。双盲判别病理分级;TRAP-ELISA法检测标本端粒酶活性。结果:各组的端粒酶阳性率分别为:A组0%、B组52.27%,C组15.38%,D组18.18%。C组、D组与B组相同时段病理分级、端粒酶阳性率差异显著(p<0.01或p<0.05);各处理组之间端粒酶活性在中度异常增生阶段差异明显。结论:GP有确切的抑制OLK癌变的功效。端粒酶可能是GP发挥抗癌作用的众多靶点之一,GP抑制端粒酶活性的最佳时相是在中度异常增生阶段。Objective： To study the dynamic effect of Gynostempa Pentaphyllum Mak （GP） on telomerase activity during Syrian golden hamsters cheek porch carcinogenesis induced by 7, 12-Dimethylbenz [αlanthracene （DMBA）. To explore the possible mechanism of GP chemoprevention to oral carcinogenesis. Method：The Salley method was used to produce the model of oral leukoplakia （OKL） carcinogenesis, and GP was used in vivo on 160 golden hamster s, ranging in age from 4 to 8 weeks old and weighing 80 to 120 grams. They were divided into 4 groups. In Group A （the control） 10 hamsters were sacrificed from 4 to 8 weeks. In Group B （the positive）, 50 hamsters were painted bilaterally on the cheeks with 0.5% DMBA 3 times a week,establishing an experimental leukoplakia group, and were sacrificed from 4 to 8 weeks. The remaining 100 hamsters were divided into 2 subgroups. Group C was the GP pre-administration group in which 50 hamsters were given GP orally for 12 weeks before DMBA painting, and this was continued during the painting period until they were sacrificed at 16 to 20 weeks. Group D was the GP post-administration group in which 50 hamsters underwent simultaneous DMBA painting and taking GP orally, and were sacrificed at 4 to 8 weeks. The double-blind method was applied to detect dynamic pathologic changes. TRAP-ELISA was used to examine the effects of GP on telomerase activity. Result：The pathology and the rates of telomerase positive were significant difference between administration group and positive group （p 〈 0.05 or p 〈 0.01）. Telomerase activity was significantly different in the different groups during the stage of moderate epithelial dysplasia （p 〈 0.05）. Conclusion： It was convincingly shown that GP inhibited OLK carcinogenesis. Telomerase activity appears to be one of many targets for the anti-carcinogenic effect of GP. The phase during which GP most inhibits telomerase activity is that of moderate epithelial dysplasia.

关 键 词：绞股蓝 口腔白斑 癌变 端粒酶 化学预防 

分 类 号：R781.5[医药卫生—口腔医学]