[Retracted] S-Nitroso-L-Cysteine Ameliorated Pulmonary Hypertension in the MCT-Induced Rats through Anti-ROS and Anti-Inflammatory Pathways

Figure 6

CSNO suppressed ROS generation, cell migration, and phosphorylation of STAT3 and ERK in vitro. (a, c) A7R5 cells were pretreated with CSNO (50 μmol/L) or NAC (5 mmol/L) for 1 hour, then stimulated with 0.5 μmol/L AngII or 25 ng/mL IL-6 for an additional 24 hours. Cytosolic ROS production was detected using the DHE fluorescence probe. (b, d) Quantification of DHE fluorescence in A7R5 cells. (e) A7R5 cells were treated with different concentrations of CSNO as indicated, and cell migration was determined by the wound healing assay. (f) Quantitative analysis of corresponding images. (g) A7R5 cells were pretreated with CSNO (50 μmol/L) for 1 hour and incubated with 0.5 μmol/L AngII for an additional 5 minutes; then, ERK1/2 phosphorylation was determined by immunoblotting. (h) Quantification of corresponding images. (i) A7R5 cells were pretreated with CSNO (50 μmol/L) for 1 hour and incubated with 25 ng/mL IL-6 for an additional 30 minutes; then, STAT3 phosphorylation was determined by immunoblotting. (j) Quantification of corresponding images. These data are calculated from three independent experiments and are displayed as . vs. controls, ^# vs. AngII or IL-6 treatment.

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