Novel Mechanisms Modulating Palmitate-Induced Inflammatory Factors in Hypertrophied 3T3-L1 Adipocytes by AMPK

Figure 6

Effects of compound C and U126 on MCP-1 in palmitate-preloaded 3T3-L1 adipocytes treated with AICAR. Adipocytes were pretreated with 10 μmol/L compound C (a, b, c, and d), 10 μmol/L U126 (e, f), or vehicle (dimethyl sulfoxide) alone for 20 min. Then, the cells were treated with 0.3 mmol/L palmitate (black bar) or vehicle (ethanol) alone (white bar) for 24 h with or without 0.5 mmol/L AICAR. Intracellular MCP-1 (d, f) was quantified by immunoblotting. AMPK phosphorylation on Thr172 (a), ACC phosphorylation on Ser79 (b), NF-κB phosphorylation on Ser536 (c), and ERK1/2 phosphorylation on Thr180/Tyr182 (e) were also quantified by immunoblot analysis. Each phosphorylation was normalized by the level of the corresponding total protein. β-actin was assessed as an internal control. Results are means ± SEM (). , compared to the corresponding controls. NS: no significant difference compared to corresponding control cells.

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