Abstract
3α-Methoxyserrat-14-en-21β-ol ( PJ-1) and 3β-methoxyserrat-14-en-21β-ol ( PJ-2) were conjugated with well-known phenolic compounds, narigenin, hesperetin, genistein, and daidzein ( 1– 8). Other conjugates of PJ-2–3,5-dihydroxy-4-methoxybenzoic acid ( 9), PJ-2–pyrogallol ( 10), and derivatives of PJ-1, PJ-2–3,3-dimethyl-succinates ( 11, 12), PJ-1, PJ-2–succinates ( 13, 14), PJ-2–glycine ( 15), PJ-2–piperidine acetic acid ( 16), and PJ-1 epoxy–3,3-dimethyl-succinate ( 17) were tested for their inhibitory effects on Epstein–Barr virus early antigen (EBV-EA) activation induced by 12- O-tetradecanoylphorbol-13-acetate (TPA). The inhibitory effects of 11 (IC 50 = 251), 12 (IC 50 = 248), and 17 (IC 50 = 230 mol ratio/32 pmol/TPA), were 2-fold stronger than those of the other compounds such as oleanolic acid (IC 50 = 449). Compounds 10, 11, and 17 inhibited mouse skin tumor promotion in an in vivo two-stage carcinogenesis model. The in vivo two-stage mouse-skin carcinogenesis test employed 7,12-dimethylbenz[a]anthracene (DMBA) as an initiator and TPA as a promoter.
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