Fig. 1.

Ginsenoside Mc1 inhibited hydrogen peroxide (H₂O₂)–mediated reactive oxygen species (ROS) production by increasing the expression of antioxidant proteins in H9c2 cells. (A) Cells were stimulated with various doses (0, 10, 25, or 50 μg/mL) of ginsenoside Mc1 for 30 min. (B) H9c2 cells were incubated with ginsenoside Mc1 (50 μg/mL) for the indicated times (0, 15, 30, or 60 min). The extent of AMPK phosphorylation was determined by Western blotting. (C) Cells were incubated with several doses (0, 25, or 50 μg/mL) of ginsenoside Mc1 for 24 h. (D) H9c2 cells were stimulated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h. Catalase and SOD2 levels were determined by Western blotting. (E) Cells were pretreated with ginsenoside Mc1 (25 or 50 μg/mL) for 24 h and then stimulated with H₂O₂ (600 μM) for 2 h. (F) H9c2 cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h and then stimulated with H₂O₂ (600 μM) for 2 h. The stimulated cells were stained with dihydroethidium (DHE) solution to assess the prevalence of intracellular ROS. The mean ± standard deviation was obtained from 3 separate experiments [*, p < 0.05; **, p < 0.005; ***, p < 0.0005; analysis of variance (ANOVA)]. AMPK, AMP-activated protein kinase; SOD2, superoxide dismutase 2.