Fig 2: Berberine enhanced AMPK signaling in macrophages upon ATP treatmentMouse macrophage J774A.1 cells, thioglycollate-elicited peritoneal macrophages (TGPMs) and bone marrow-derived macrophages (BMDMs) were treated as described in Figure 1 and Figure 2, respectively. Western blotting was used to assess protein expression in the cell lysates A. ß-Tubulin was recruited as a loading control. Quantifications of p-AMPKa relative to AMPKa are shown in B., while quantifications of AMPKa relative to ß-tubulin are shown in C., respectively (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant; BBR, berberine.

Fig 3: Altered phosphorylation of downstream signaling molecules in APN-KO mice. Representative immunoblots showing (A) pAMPK/AMPK relative densities (B) pGSK3ß/GSK3ß relative densities and (C) pCREB/CREB relative densities, in total hippocampal lysate. Forty micrograms of protein were loaded per lane. Bars represent mean ± SEM; *p < 0.05, **p < 0.01; n = 4 mice per group.

Fig 4: Western blotting revealed that cardiac p-AMPK and p-NF-kB P65 was activated and suppressed by SH treatment, respectively. Sham, n = 6; MI, n = 6; MI+LSH, n = 6; MI+HSH, n = 6. Data were expressed as means ± SD. ?Compared with Sham group, p < 0.05; *compared with MI group, p < 0.05; #compared with MI+LSH group, p < 0.05.

Fig 5: Western blotting showed that SH decreased the expression of inflammatory cytokines, increased the activation of AMPK, suppressed the activation of NF-kB P65 on H9C2 post COCl2-induced hypoxia. Control, n = 6; 0, CoCl2 + 0 µ/ml SH, n = 6; 10, CoCl2 + 10 µg/ml SH, n = 6; 20, CoCl2 + 20 µg/ml SH, n = 6; 30, CoCl2 + 30 µg/ml, n = 6. *Compared with control, p < 0.05; #compared with 0 µg/ml SH post CoCl2, p < 0.05; ?compared with 10 µg/ml SH post CoCl2, p < 0.05; &compared with 20 µg/ml post CoCl2, p < 0.05.