Fig. 1

Mangafodipir inhibits apoptosis in granulosa cells induced by H₂O₂ and anticancer drugs. a A MTS assay was performed after treatment with H₂O₂ (0, 0.1, or 1 mM) without (m0) or with the administration of mangafodipir (40 μM: m40; 200 μM: m200; 1000 μM: m1000). Mean ± SEM, *, p < 0.01 vs. each control (m0). b Apoptosis was assessed via immunoblotting using anti-cleaved caspase-3 antibody. Mangafodipir did not increase cleaved caspase-3 levels (upper panels). Cleaved caspase-3 induced by 1 mM H₂O₂ was suppressed by the simultaneous addition of 1000 μM/L mangafodipir (lower panels). c The relative intensity of cleaved caspase-3 (CC3) to β-actin was measured to assess the results of the immunoblot in the H₂O₂ in vitro experiments. Mean ± SEM, *, p < 0.01 vs. each control (m0). d A MTS assay was performed after 48-h treatment with 10 or 60 μM cisplatin (CIS) or 10 or 50 μM paclitaxel (PTX) with mangafodipir (200 μM: m200; 1000 μM: m1000) or without mangafodipir (m0). Mean ± SEM, *, p < 0.05 vs. each control (m0). e Apoptosis was assessed via immunoblotting using anti-cleaved caspase-3 antibody. Cleaved caspase-3 was induced with 10 or 60 μM cisplatin (CIS) and 10 μM paclitaxel (PTX) and was suppressed by the simultaneous addition of 1000 μM mangafodipir. f The relative intensity of cleaved caspase-3 (CC3) to β-actin was measured to assess the results of the immunoblot in the anticancer drug-based in vitro experiments. Mean ± SEM, *, p < 0.05 vs. each control (m0). g ROS production was assessed by immunoblotting using anti-4HNE antibody. 4-HNE induced by 10 or 60 μM cisplatin (CIS) or 10 or 50 μM paclitaxel (PTX) was suppressed by the simultaneous addition of 200 μM and 1000 μM mangafodipir. h The relative intensity of 4-HNE to β-actin was measured to assess the results of immunoblotting in anticancer drugs in vitro experiments. Mean ± SEM, *, p < 0.05 vs. each control (m0)