云芝糖肽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  

The study of Yun Zhi Polysaccharopeptide chemoprevention on altered telomerase activity during golden hamster cheek pouch carcinogenesis

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6期372-375,共4页Journal of Clinical Stomatology

基　　金：国家自然科学基金资助(39870928)

摘　　要：目的:探讨中药云芝糖肽(Yun Zhi Polysaccharopeptide,PSP)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PSP作为癌化学预防药物的可能药理机制。方法:以Salley法建立金地鼠颊囊癌变模型,PSP进行体内干预,110只金地鼠分4组:空白对照组(A组);模型对照组(B组);先、后服用PSP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8.7%,D组26.92%。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:PSP有确切的抑制实验性口腔白斑癌变的功效。端粒酶可能是PSP发挥癌化学预防作用的众多靶点之一,PSP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 intervention and dynamic effect of Yun Zhi Polysaccharopeptide （PSP） on telom-erase activity during cheek pouch carcinogenesis induced in Syrian golden hamsters by 7, 12-Dimethylbenz [alpha]an-thracene （DMBA）, and to explore the possible mechanism of PSP chemoprevention to oral carcinogenesis. Method：The Salley method was used to produce the model of oral leukoplakia （OKL） carcinogenesis, and PSP was used in vivo on 110 golden hamsters,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,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 50 hamsters were divided into 2 subgroups. Group C was the PSP pre-administration group in which 25 hamsters were given PSP 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 PSP post-administration group in which 25 hamsters underwent simultaneous DMBA painting and taking PSP orally, and were sacrificed at 4 to 8 weeks. The double-bllnd method was applied to detect dynamic pathologic changes. TRAP-ELISA was used to examine the effects of PSP on telomerase activity. Result：The pathology and rates of telomerase positivity were significantly different in the administration groups and the control group （p 〈 0.05;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 PSP inhibited OLK carcinogenesis. Telomerase activity appears to be one of many targets for the anti-carcinogenic effect of PSP. The phase during which PSP most inhibits telomerase activity is that of moderate epithelial dysplasia.

关 键 词：云芝糖肽 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]