Chemopreventive effect of green tea catechin on rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide

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  • Kono Takako
    Graduate School of Dentistry (First Department of Oral and Maxillofacial Surgery), Osaka Dental University
  • Matsushima Yuki
    First Department of Oral and Maxillofacial Surgery, Osaka Dental University
  • Morita Shosuke
    First Department of Oral and Maxillofacial Surgery, Osaka Dental University

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Oral cancer treatment may have significant adverse effects on the patient's activities of daily living (ADL) and quality of life (QOL). In recent years attention has been focused on the use of food for chemoprevention. (-)-Epigallocatechin-3-gallate (EGCG), which accounts for about half of green tea catechins, is not only a strong antioxidant, but has also been reported to possess anti-tumor and carcinogenesis-inhibiting actions. As the oral mucosa comes into direct contact with green tea, its carcinogenesis-inhibiting action may be effective against oral cancer. We investigated the carcinogenesis-inhibiting activity of EGCG in the carcinogenic process in rats with tongue cancer induced by 4-nitroquinoline 1-oxide (4NQO). Sprague-Dawley (SD) rats were given water containing either a 50-ppm aqueous solution of 4NQO to induce tongue cancer or the 4NQ0 solution together with a 500-ppm aqueous solution of EGCG. A control group was given only distilled water. Macroscopic observations and histopathologic comparisons were made of the back of the tongue at 8, 12, 16, 20 and 24 weeks after the start of administration. The association between activated nuclear factor κB (NF-κB) p65 and IκB kinase α (IKKα) expression and tumor growth in the carcinogenic process was investigated by immunohistochemical staining and immunoblotting. The administration of EGCG not only significantly suppressed the occurrence of epithelial dysplasia and squamous cell carcinoma in rats with 4NQO-induced tongue cancer, but also inhibited the expression of activated (NF-κB) p65 and IKKα (p<0.05). It also decreased the proportion of Ki-67-positive cells, and inhibited cell proliferative activity (p<0.05). Western blotting was performed for these proteins, and the same results were also obtained for their expression via immunostaining. These results suggest that the carcinogenesis-inhibiting action of EGCG is probably due to the inhibition of activated NF-κB p65, and that long-term administration of EGCG may decrease IKKα expression, increasing its activity in suppressing the promotion of carcinogenesis and suppressing multi-step carcinogenesis.

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