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Figure 7 | Molecular Medicine

Figure 7

From: Activation of AMPK Enhances Neutrophil Chemotaxis and Bacterial Killing

Figure 7

Effects of metformin, AICAR and IKK inhibitor on LPS-dependent activation of TLR4 or mTOR signaling pathways. Neutrophils were cultured with AICAR (0 or 500 µmol/L) for 2.5 h, metformin (0 or 500 µmol/L) for 2.5 h, IKK inhibitor PS-1145 (0 or 10 µmol/L) for 60 min or rapamycin (0 or 30 nmol/L) for 30 min. Next, neutrophils were cultured with LPS (0 or 300 ng/mL) for an additional 60 min. (A, C, F, G) Representative Western blots show amount of IκBα, total and phosphorylated ribosomal protein S6 (rpS6) (Ser240/244), 4E-binding protein 1 (4E-BP1), and actin. Panels (B, D, F and H) show average of Western blots optical bend densitometry. Means ± SEM (n = 3); (B, D) *P < 0.05, **P < 0.01 compared with LPS only; (F) **P< 0.01 compared with control (untreated); (H) **P< 0.01 compared with control (untreated), LPS or rapamycin- and LPS-treated cells. Panel (E) shows the ability of IKK inhibitor PS-1145 to prevent LPS-mediated inhibition of neutrophil chemotaxis.

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