Fig. 5

Genistein induced mitochondrial respiration and suppressed pro-inflammatory state in macrophage. a Mitochondrial respiration analysis of control and genistein groups (1 μM, 18 h). A: Basal respiration, B: ATP production, C: Proton Leak, D: Maximal respiration, E: Non-mitochondrial respiration, F: Spatial respiratory capacity. b Western blot analysis and quantification of phospho-AMPKα. Genistein (1 μM) was treated for 6 h. Beta actin was used as an internal control. (c) qRT-PCR analysis of pro-inflammatory cytokines. Genistein (1 μM) was treated for 6 h. Rplp0 was used as an internal control. d Western blot analysis and quantification of phospho-AMPKα and p53. LPS (100 ng/ml) was treated for 3 h and genistein (1 μM) was pre-treated for 2 h. Beta actin was used as an internal control. (e) qRT-PCR analysis of IκBα and pro-inflammatory cytokines in Raw 264.7 cell. Rplp0 was used for an internal control. Genistein (1 μM) was pre-treated 1 h before LPS incubation (100 ng/ml, 3 h). Values represent means ± SEM of at least 3 experiments. *, P < 0.05