Objective: To investigate the molecular mechanism by which salidroside protects PC12 cells from HO-induced apoptosis.
Methods: 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 HO 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 and p47 in the membrane and cytoplasm were detected by membrane-cytoplasm separation experiment; the binding between gp91 and p47 was assayed by coimmunoprecipitation experiment.
Results: Salidroside dose-dependently suppressed cell apoptosis, lowered phosphorylation levels of p38, ERK and JNK, inhibited the production of ROS, reduced the binding between gp91 and p47, and inhibited the activity of NOX2 in PC12 cells exposed to HO.
Conclusion: Salidroside protects PC12 cells from HO-induced apoptosis at least partly by suppressing NOX2-ROS-MAPKs signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779671 | PMC |
| http://dx.doi.org/10.3969/j.issn.1673-4254.2017.02.06 | DOI Listing |
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