Figure 5.

Clau F induced neurite outgrowth by activating the ERK pathway, but not the AKT pathway, in PC12 cells. Quantitative analysis of band density was performed using three independent Western blotting analyses. (A) In the Clau F group (b-d), the ERK-specific inhibitor PD98059 completely abolished neurite outgrowth, whereas the PI3K-specific inhibitor LY294002 only reduced neurite outgrowth by 14.4%. In the NGF group (e–h), single treatment with PD98059 or LY294002 did not cause significant changes in the ratio of neurite outgrowth; only co-treatment with PD98059 and LY294002 successfully abolished the neurite outgrowth promoted by NGF. Morphological changes were observed with an inverted microscope. (B) The expression of GAP-43 was significantly decreased in the PD98059 group, whereas it was only attenuated by 13% in the LY294002 group. (C) The levels of phospho-CREB and acetylated p53 were significantly decreased by the ERK-specific inhibitor PD98059. The PI3K-specific inhibitor LY294002 decreased the level of phospho-CREB by 13.3% and acetylated p53 by 19.0%. Mean±SEM. ^bP<0.05, ^cP<0.01 vs control. β-Actin protein was used as a loading control.