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. 2013 Feb 4;110(8):3161–3166. doi: 10.1073/pnas.1222051110

Fig. 5.

Fig. 5.

AMPK regulates Bcl-6 transactivation and the subsequent repression of VCAM-1, MCP-1, MCP-3 in vivo. (A and B) AMPK+/+ and AMPKα2−/− mice were injected with saline (Ctrl) or metformin (200 mg/kg) for 5 h. (A) The level of PARP-1 binding to the Bcl-6 intron 1 in extracted aortic tissues was analyzed using ChIP followed by qPCR. (B) The levels of Bcl-6 mRNA and protein were assessed using qPCR and immunoblotting, respectively. (C and D) AMPK+/+ and AMPKα2−/− mice were injected with TNF-α (25 µg/kg) alone for 5 h or with TNF-α (25 µg/kg) for 1 h followed by metformin (200 mg/kg) for 4 h. (C) The level of Bcl-6 binding to the promoters of VCAM-1, MCP-1, and MCP-3 in extracted aortic tissues was assessed using ChIP analysis followed by qPCR. (D) mRNA levels for VCAM-1, MCP-1, and MCP-3 were then assessed in the aorta using qPCR. (E) A graphic illustration of the anti-inflammatory effect of the AMPK–PARP-1–Bcl-6 pathway.