Fig. 3

AA inhibits pro-inflammatory cytokine secretion through suppression of NF-κB, STAT3, and ERK pathway in METH-stimulated SH-SY5Y cells. SH-SY5Y cells were pretreated with 20 μM AA or various inhibitors for 1 h and then stimulated with 1 mM METH for 24 h. a Phosphorylation of ERK was strongly inhibited in METH-stimulated SH-SY5Y cells by AA administration. Inhibitors of NF-κB (Bay11-7085), STAT3 (S3I-201), ERK (PD98059), or AA strongly suppressed METH-induced TNFα and IL-6 production both in extracellular (b) and mRNA levels (c, d). METH-induced translocation of p65 and STAT3 was inhibited when the ERK pathway of these cells were downregulated. β-actin and lamin B were used to confirm equal sample loading. Immunoblotting was quantified by densitometric analysis. The data are representative of three independent experiments and quantified as mean values ± SEM (n = 4 to 6). Tukey’s multiple comparison test, *p < 0.05 compared to normal control, ^† p < 0.05 compared to METH treatment