Abstract: A stable GPR41 receptor cell line was used to screen candidate agonist from the secondary metabolites extracted from gulf seaweed aflatoxin c-f-3 in Putian Fujian. The cAMP results have shown that the No.17 compound Cyclo (L-Pro-L-Phe), belonging to cyclic dipeptide, is able to increase intracellular cAMP in a variety of cells (including G41-CHO, G12-CHO, Mock-CHO, SH-sy5y and HEK293). We have demonstrated that No.17 compound induced cAMP increase in a GPCR-independent manner. Co-adminstration of adenylate cyclase activating agent forskolin and No.17 compound can lead to a further increase in cAMP level compared with those treated with forskolin alone. These results have suggested that No.17 compound may induce a sustained elevation of cAMP levels by inhibiting cAMP hydrolysis. Since No.17 compound shared similar chemical structures with some known PDE inhibitors, which may be a potential of phosphodiesterase inhibitors. This is the first report that Cyclo(L-Pro-L-Phe) could regulate cAMP formation in a variety of cells (G41-CHO, G12-CHO, Mock-CHO, SH-sy5y and HEK293).

Key words: secondary metabolites of marine fungi, cAMP, Cyclo(L-Pro-L-Phe), phosphodiesterase inhibitor