HMGB1 Is Involved in the Protective Effect of the PPARα Agonist Fenofibrate against Cardiac Hypertrophy
Figure 1
Fenofibrate inhibits the basal and LPS-induced expression of HMGB1. (a) and (b) Fenofibrate induces time-dependent inhibition of the expression of HMGB1 in primary cardiomyocytes at the mRNA level (a) and protein level (b). Cells were treated with 10 μM fenofibrate for 12, 24, 36, 48, and 60 h before being used for experiments. (c) and (d) Fenofibrate-induced concentration-dependent inhibition of the expression of HMGB1 in primary cardiomyocytes at the mRNA level (c) and protein level (d). Cells were treated with 1, 10, and 100 μM fenofibrate for 36 h before experiments. (e) and (f) Fenofibrate inhibited basal and LPS-induced HMGB1 expression in cardiomyocytes as determined by real-time PCR (e) and western blot (f). Cells were treated with the DMSO vehicle or the same dose of fenofibrate at a final concentration of 10 μM for 36 h; LPS (50 ng/mL) was then added and incubated for 10 h. (g) Fenofibrate inhibits basal and LPS-induced secretion of HMGB1 in cardiomyocytes; similar treatments were performed as described for (e) and (f), and the HMGB1 level was analyzed by ELISA. All the data are representative of at least three independent experiments, and the data in (a), (c), (e), and (g) are presented as the mean ± SEM. versus DMSO vehicle and versus LPS alone.
