Fig 1: LY294002 treatment and the knockdown of PGC-1a and PGC-1ß antagonize the effect of IGF-I on NOZ cell colony formation and invasion. (A) The cell colony formation ability elevated by IGF-I was significantly decreased by LY294002 and the knockdown of PGC-1a and PGC-1ß. (B) The elevated invasive capacity of NOZ cells by IGF-I was antagonized by LY294002 and the knockdown of PGC-1a and PGC-1ß. Magnification, ×20. All of the experiments were conducted in triplicate. *P<0.05, **P<0.01. IGF-I, insulin-like growth factor I; PGC1-1, peroxisome proliferator-activated receptor-? coactivator-1; NC, negative control; sh, short hairpin RNA; NS, not significant.
Fig 2: PI3K/AKT phosphorylation activates ERRa. (A) The inhibition of the PI3K/AKT phosphorylation by LY294002 effectively decreased the activity of ERRa. (B) PI3K/AKT phosphorylation induced by IGF-I effectively enhanced the activity of ERRa. (C) LY294002 treatment antagonized the upregulated ERRa activity induced by IGF-I. (D) The knockdown of ERRa antagonized the upregulated ERRa activity caused by IGF-I. (E) Protein expression levels of PGC-1a and PGC-1ß were notably elevated by IGF-I. The expression levels of PRC and ERRa were not affected. (F) The protein expression levels of PGC-1a and PGC-1ß were reduced by LY294002, while those of PRC and ERRa were not altered. All of the experiments were repeated three times. **P<0.01. IGF-I, insulin-like growth factor I; ERE, estrogen response element; ERR, estrogen-related receptor; PGC1-1, peroxisome proliferator-activated receptor-? coactivator-1; PRC, PGC-related coactivator; NC, negative control; sh, short hairpin RNA.
Fig 3: BAC activated AMPK/PGC-1 axis in OGD/R-treated H9C2 cells.Western blot analysis was utilized for evaluating the protein levels of AMPK, p-AMPK, and PGC-1α. ***p < 0.001 indicates the difference compared with control group; #p < 0.05 indicates the difference compared with OGD (2 h)/R (6 h) + BAC (0 μM) group; ###p < 0.001 indicates the difference compared with OGD (2 h)/R (6 h) + BAC (0 μM) group. BAC, benzoylaconine; OGD (2 h)/R (6 h), oxygen-glucose deprivation (2 h) and reperfusion (6 h); SOD, superoxide dismutase.
Fig 4: Knockdown of PGC-1a and PGC-1ß attenuates the effect of IGF-I on ERRa. (A) Lv-shPGC-1a and (B) Lv-shPGC-1ß effectively knocked down PGC-1a and PGC-1ß, respectively. Knockdown of (C) PGC-1a and (D) PGC-1ß attenuated the upregulated activity of ERRa caused by IGF-I. (E) LY294002 treatment and knockdown of (F) PGC-1a and (G) PGC-1ß reduced NOZ cell viability that was enhanced by IGF-I. All of the experiments were conducted in triplicate. *P<0.05, **P<0.01. IGF-I, insulin-like growth factor I; ERE, estrogen response element; ERR, estrogen-related receptor; PGC1-1, peroxisome proliferator-activated receptor-? coactivator-1; NC, negative control; sh, short hairpin RNA; NS, not significant.
Fig 5: Effect of P. umbrosa root extract on lipid accumulation and browning-specific gene expression in 3T3-L1 adipocytes. (A) Oil red O staining (×200); (B) Lipid accumulation (%); (C) Browning-specific gene expression. (B,C) Data are presented as means ± SEM. Significant differences between CON (MDI+) and PUE are indicated by * p < 0.05; ** p < 0.01. MDI-, MDI-untreated cells; CON (MDI+), MDI-treated cells; PUE, MDI + P. umbrosa root extract, 100 µg/mL. MDI, methylisobutylxanthine, dexamethasone, and insulin; Pgc1a, Peroxisome proliferator-activated receptor gamma co-activator 1-alpha; Ucp1, Uncoupling protein 1; Prdm16, PR domain containing 16; Cpt1a, Carnitine palmitoyl-CoA transferase 1-alpha.
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