Fig. 8.

Role of PPARα in FAAH inhibitor-induced, endocannabinoid-induced, or endocannabinoid-like substance-induced p42/44 MAPK activation. A, B: MSCs were pretreated with the PPARα antagonist GW6471 (10 μM) for 1 h and subsequently incubated with vehicle, URB597 (A; 10 μM, additional 2 h treatment) or AA-5HT (B; 10 μM, additional 1 h treatment). C: MSCs were pretreated with the PPARα antagonist GW6471 (GW) (10 μM) for 1 h and subsequently incubated with vehicle or the indicated endocannabinoids or endocannabinoid-like substances (EC) [AEA, 2-AG, OEA, or PEA (all at 10 μM)] for an additional 1 h incubation period. Histograms above the blots indicate activation of p42/44 MAPK determined by densitometric analyses of phosphorylated p42/44 MAPK normalized to that of nonphosphorylated p42/44 MAPK. β-actin was used as loading control. Data represent mean ± SEM compared with vehicle control (100%) of n = 5 experiments with cells from three donors (A), n = 6 experiments with cells from two donors (B), n = 6 experiments with cells from three donors (C, left panel), n = 6 experiments with cells from two donors (C, right panel). *P < 0.05 versus vehicle, one-way ANOVA plus post hoc Bonferroni test.