[Salidroside protects PC12 cells from H₂O₂-induced apoptosis via suppressing NOX2-ROS-MAPKs signaling pathway]

To investigate the molecular mechanism by which salidroside protects PC12 cells from H₂O₂-induced apoptosis.

PC12 cells cultured in DMEM supplemented with 10% horse serum and 5% fetal bovine serum were pretreated with different doses of salidroside for 2 h and then stimulated with H₂O₂ for different lengths of time. The expression levels of PARP and caspase 3 and the phosphorylation of p38, ERK and JNK were determined with Western blotting. The cell nuclear morphology was observed after DAPI staining. The production of ROS was detected using a ROS detection kit, and the levels of gp91^phox and p47^phox in the membrane and cytoplasm were detected by membrane-cytoplasm separation experiment; the binding between gp91^phox and p47^phox was assayed by coimmunoprecipitation experiment.

Salidroside dose-dependently suppressed cell apoptosis, lowered phosphorylation levels of p38, ERK and JNK, inhibited the production of ROS, reduced the binding between gp91^phox and p47^phox, and inhibited the activity of NOX2 in PC12 cells exposed to H₂O₂.

Salidroside protects PC12 cells from H₂O₂-induced apoptosis at least partly by suppressing NOX2-ROS-MAPKs signaling pathway.