Fig. 2.

Increased anti-apoptotic effects of PPARβ/δ-primed MSC on cardiomyocytes. a After 24 h of MSC pharmacological preconditioning using PPARβ/δ agonist, cells were co-cultured in classical culture medium (CM) using transwells (upper chamber) with H9c2 (lower chamber) previously exposed to 350 µM of H₂O₂ in minimal medium (serum deprivation) during 4 h. At the end of the protocol, specific DNA fragmentation was quantified in H9c2 cells and values were compared with those obtained for co-cultures with naive MSC or MSC pre-treated with PPARβ/δ antagonist (GSK0660). b Scatter dot plot and bars were presented for specific DNA fragmentation quantified in H9c2 at the end of the protocols. Data (mean ± SD for each group of treatment) were normalized by values obtained with H9c2 (not challenged by H₂O₂) and compared among groups performed using Kruskal–Wallis with the Dunn’s post hoc test for multiple comparison. On the top of each bar, P values were noted for the comparison vs H9c2/H₂O₂ first and second vs MSC. P values vs H9c2/H₂O₂ were noted ns for p > 0.999 (naïve MSC), **** for p < 0.0001 (0.1 µM GW0742), vs ** for p = 0.073 (1 µM GW0742), * for p = 0.0402 (vs 0.1 µM GSK0660) and ns for p = 0.0582 (MSC/H₂O₂ vs 1 µM GSK0660). Significance compared to naïve MSC was noted ** for p = 0.0058 (0.1 µM GW0742), ns for p = 0.3642 (for 1 µM GW0742) and ns for p > 0.999 (for GSK0660 at both doses)