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

Figure 2

Effects of AICAR on palmitate-induced MCP-1, NF-κB, and MAPK signaling in 3T3-L1 adipocytes. 3T3-L1 cells were exposed to 0.3 mmol/L palmitate (black bar) or ethanol vehicle alone (white bar) in the presence or absence of 0.5 mmol/L AICAR for 12 h. The mRNA levels of MCP-1 were measured by quantitative real-time RT-PCR (a). After additional 12 h, cell lysates were immunoblotted to determine the intracellular MCP-1 concentration (b), phosphorylation of NF-κB on Ser536 (d), ERK1/2 on Thr180/Tyr182 (e), p38 MAPK on Thr180/Tyr182 (f), and JNK on Thr183/Tyr185 (g). β-Actin was measured as an internal control, and each phosphorylation was normalized by the corresponding total protein concentration. The release of MCP-1 was also assessed by ELISA (c). Data are means ± SEM (). , compared to corresponding control cells. NS: no significant difference compared to corresponding control cells.

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