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. 2007 Oct 2;104(41):16329–16334. doi: 10.1073/pnas.0706662104

Fig. 4.

Fig. 4.

Gambogic amide provokes MAPK and Akt kinase activation and neurite outgrowth. (A) Gambogic amide selectively provokes Erk phosphorylation in T17 cells, whereas other derivatives exhibited weakly stimulatory effects. By contrast, in addition to gambogic amide, GA and decahydro-GA also triggered robust Akt activation. (B) GA derivatives initiate Akt activation in hippocampal neurons. (C) Characterization of gambogic amide's stimulatory effect on Akt phosphorylation. (Left) Then 500 nM gambogic amide elicited Akt activation in a time-dependent manner. (Right) Gambogic amide induced Akt activation in a dose-dependent manner during 30-min treatment. (D) PC12 cells were treated with NGF or 0.5 μM GA derivatives for 5 days. Gambogic amide triggered neurite outgrowth as potently as NGF, and dihydro-GA also displayed weak stimulatory activity. By contrast, other derivatives had no effect. (E) Dose-dependent effect of neurite outgrowth. Further, 10–50 nM gambogic amide can provoke neurite outgrowth in PC12 cells. (F) K252a abolishes gambogic amide-provoked neurite outgrowth in PC12 cells.