Fig. 4
MA-5 protected cells from mitochondrial oxidative stress and allowed energy production. a and b Cellular ROS levels were determined via flow cytometry in control cells (Ctrl), and in cells treated with 10 ng/ml TNFα (TNFα), 10 ng/ml TNFα and 5 μM MA-5 (TNFα+MA-5), or 10 ng/ml TNFα and 5 μM MA-5 after silencing of Bnip3 with an siRNA (TNFα+MA-5 + si-Bnip3). c through e The level of GSH and the activities of SOD and GPx were measured via ELISA in control cells (Ctrl), and in cells treated with 10 ng/ml TNFα (TNFα), 10 ng/ml TNFα and 5 μM MA-5 (TNFα+MA-5), or 10 ng/ml TNFα and 5 μM MA-5 after silencing of Bnip3 with an siRNA (TNFα+MA-5 + si-Bnip3). f ATP production increased in response to MA-5 treatment and decreased after Bnip3 was silenced. g through j The alterations in mitochondrial respiratory complexs in control cells (Ctrl), and in cells treated with 10 ng/ml TNFα (TNFα), 10 ng/ml TNFα and 5 μM MA-5 (TNFα+MA-5), or 10 ng/ml TNFα and 5 μM MA-5 after silencing of Bnip3 with an siRNA (TNFα+MA-5 + si-Bnip3). *p < 0.05 vs. control (Ctrl) group; #p < 0.05 vs. TNFα group; †p < 0.05 vs. TNFα+MA-5 group