Objective: To study the intervention and dynamic effect of Gynostema Pentaphyllum Mak (GP) on telomerase activity during cheek pouch carcinogenesis induced in Syrian golden hamsters by 7,12-Dimethylbenz[alpha]anthracene DMBA, and to explore the possible mechanism of suppression of oral carcinogenesis of GP. Methods: The Salley method was used to produce the model of oral leukoplakia OKL carcinogenesis, and GP was used in vivo on 144 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) 9 hamsters were sacrificed from 4 to 8 weeks. In Group B, 45 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 90 hamsters were divided into 2 subgroups. Group C was the GP pre-administration group in which 45 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 45 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. Results: 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 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.