DMBA诱发的地鼠口腔癌发病机制研究  

STUDY ON DMBA-INDUCED HAMSTER ORAL CARCINOGENIC MECHANISMS

作　　者：李宁[1] 陈晓欣[2] 韩驰[1] 陈君石[1] 杨中枢[2] 

机构地区：[1]中国疾病预防控制中心营养与食品安全所,北京100050 [2]Rutgers大学,美国新泽西08854

出　　处：《癌变．畸变．突变》2003年第1期21-24,T002,共5页Carcinogenesis,Teratogenesis & Mutagenesis

摘　　要：目的 :用DMBA诱发的地鼠口腔癌模型 ,探讨口腔癌的发病机制。 方法 :0.5 %DMBA涂于地鼠左侧颊囊 ,每周3次 ,共涂6周 ,观察至24周 ;用免疫组化方法检测口腔不同病变包括正常粘膜、单纯增生、异常增生、乳头状瘤和癌组织中Brdu标记指数和血管密度 ,并以形态学方法记数凋亡细胞 ,计算凋亡指数。 结果 :Brdu标记指数和血管密度均随着口腔癌病变的发展而增高 ,与病变呈正相关。细胞凋亡指数从正常粘膜、单纯增生到异常增生、乳头状瘤和癌组织增高 ,但异常增生、乳头状瘤和癌组织之间无显著性差异。 结论Purpose: To explore the carcinogenic mechanisms of oral cancer in DMBA_induced hamster. Methods: 0.5 % DMBA solution (in mineral oil) was applied topically to the left cheek pouch of male Syrian golden hamsters 3 times per week for 6 weeks, and the animals were observed until the 24 th week. Brdu_labelling index and vascular density were examined by immunostaining in different oral lesions including normal mucosa, hyperplasia, dysplasia, papilloma and squamous cell carcinoma(SCC) . Apoptotic cells were evaluated based on morphological features. Results: Brdu_labeling index and vascular density increased with oral carcinogenesis, and were correlated with oral histopathological grades. Apoptotic index increased from normal mucosa and hyperplasia to dysplasia, papilloma and SCC, but there was no significant difference among dysplasia, papilloma and SCC. Conclusion: Cell proliferation and angiogenesis are the important carcinogeneic mechanisms of oral cancer.[

关 键 词：地鼠 口腔癌 增殖 凋亡 新生血管 二甲基苯并蒽 

分 类 号：R781[医药卫生—口腔医学]