YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission

Figure 4

YQFM protects against H₂O₂-induced mitochondrial dysfunction and apoptosis. Neurons were pretreated with YQFM (100, 200, and 400 μg/ml) or NAC (500 μM) for 6 h before exposure of H₂O₂ (100 μM) for 12 h. (a) Intracellular ROS level was detected in neurons stained with DCFH-DA. Bar = 100 μm. (b) Mitochondria-derived ROS generation was determined using a mitochondrial superoxide anion specific fluorescent probe (MitoSOX red). The fluorescence was measured using a fluorometer. (c) Cellular ATP content was measured by an ATP assay kit. (d) Mitochondrial membrane potential was evaluated by TMRE using a fluorometer. Protein expression of Bcl-2 (e), Bcl-xl (f), Bax (g), and Bak (h) was detected by Western blot. Data were presented as mean ± SD from three independent experiments. versus control, versus H₂O₂, versus H₂O₂.

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