Fig 2: Expression levels of Angptl4 and analysis of PPAR-α activity in the I/R-injured diabetic hearts treated with or without TXL in the presence or absence of signal regulators.(A) Angptl4 expression was decreased by I/R injury, and pre-treatment with insulin, rhAngptl4, or TXL reverted this effect. Whereas, Angptl4 siRNA and MK886 abolished the TXL-induced upregulation of Angptl4. (B) I/R injury decreased the PPAR-α activity in the I/R-injured myocardium, and even worse in diabetic hearts. Pre-treatment of insulin, rhAngptl4 and TXL increased the PPAR-α activity. Addition of MK886 but not Angptl4 siRNA abolished the TXL-stimulated PPAR-α activation. Compared with the DB-sham group, *P<0.05, **P<0.01; Compared with the DB-MI group, †P<0.05, ††P<0.01; Compared with the TXL group, ‡P<0.05, ‡‡P<0.01; Compared with the rhAngptl4+siR group, §§P<0.01. Abbreviations as in Fig 1.

Fig 3: The activity of PPAR-α in different cells: (A) the effects of BP on the antagonist of PPAR-α in HL7702 cells; and (B) the effects of BP on the antagonist of PPAR-α in HepG2 cells. Five samples were analyzed in each group. All data are presented as mean value ± S.D. * p < 0.05 via a blueberry juice group BG.

Fig 4: Real-time quantitative RT-PCR analysis of the mRNA levels of SREBP-1c/PNPLA-3 pathway and its interacting molecules. (A) Relative mRNA level of PPAR-α; (B) Relative mRNA level of SREBP-1C; (C) Relative mRNA level of PNPLA3. Eight liver samples were analyzed in each group. All data are presented as mean value ± S.D. * p < 0.05 via a blueberry juice group BG.

Fig 5: The effects of PPAR-α antagonist and blueberry juice on the growth of human liver cells: (A) the effects of PPAR-α antagonist and blueberry juice on the growth rate of cell line HL7702; and (B) the effects of PPAR-α antagonist and blueberry juice on the growth rate of liver cell line HepG2. All data are presented as mean value ± S.D. Five samples were analyzed in each group. * p < 0.05 via a blueberry juice group.