726
Figure 2.- Viability % inhibition effect of 40 µM curcumin for different periods ranged from
(4-24h) on 3T3-L1 adipocytes. Cells Viability % was calculated by formula sample/control)
x100.
3.3. Curcumin induces AMPK and adiponectin activation and suppresses PKA
and CREB phosphorylation.
We next studied downstream the effect of Curcumin on these signals.
Western blot analysis demonstrated that cells treated with 40 μM curcumin
induced AMPK phosphorylation (p-AMPK) and reduced levels of phosphorylated
CREB (p-CREB) and phosphorylated Akt (p-Akt, to a lesser extent). Curcumin
increased the expression of adiponectin, however, total AMPK expression was
unaffected. β-actin was used as a loading control (Figure 4).
3.4. Curcumin inhibits PKA activation.
We further demonstrated a gradual decrease with time in the expression of
the PKA catalytic subunit, an important transcription factor. The results of the PKA
relative phosphorylation assay support this result; PKA relative activity was
inhibiting 4–24-h post-curcumin treatment (Figure 5B)
