Salidroside protects PC12 cells from HO-induced apoptosis via suppressing NOX2-ROS-MAPKs signaling pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the molecular mechanism by which salidroside protects PC12 cells from HO-induced apoptosis.</p><p><b>METHODS</b>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 HOfor 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 gp91and p47in the membrane and cytoplasm were detected by membrane-cytoplasm separation experiment; the binding between gp91and p47was assayed by coimmunoprecipitation experiment.</p><p><b>RESULTS</b>Salidroside dose-dependently suppressed cell apoptosis, lowered phosphorylation levels of p38, ERK and JNK, inhibited the production of ROS, reduced the binding between gp91and p47, and inhibited the activity of NOX2 in PC12 cells exposed to HO.</p><p><b>CONCLUSION</b>Salidroside protects PC12 cells from HO-induced apoptosis at least partly by suppressing NOX2-ROS-MAPKs signaling pathway.</p>

Effect of sodium aescinate in inducing human breast cancer MCF-7 cells apoptosis by inhibiting AKT, ERK and upstream signal SRC activity / 中国中药杂志

To study the effect of sodium aescinate in inducing human breast cancer MCF-7 cells apoptosis and its possible mechanism. MTT assay was used to detect the inhibitory effect of sodium aescinate on the proliferation of MCF-7 cells. The morphological changes were observed under inverted microscope. DAPI nuclear staining was used to detect the changes in cell nucleus. Annexin V-FITC/PI flow cytometry was adopted to test the apoptosis rate. Changes in apoptosis-related proteins (PARP, cleaved caspase-8 and pro-caspase-3), cell survival-associated signal molecules (AKT and ERK) and their common upstream kinase SRC was detected by Western blotting. The result showed that after different concentrations of sodium aescinate were used to treat breast cancer MCF-7 cells, they inhibited the proliferation of MCF-7 cells in a dose-dependent manner, induced cell apoptosis (typical morphological changes in nucleus, significant increase in cell apoptosis rate). The expressions of cleaved PARP and caspase-8 increased, while the expression of pro-caspase-3 decreased, which further verified sodium aescinate's effect in inducing cell apoptosis. Sodium aescinate significantly inhibited the phosphorylation of cell survival-related signal molecules (AKT, ERK) and down-regulate the activation of their common up-stream kinase SRC. The findings indicated that sodium aescinate can block signals transiting to downstream molecules AKT, ERK, inhibit the proliferation of breast cancer cell MCF-7 cell apoptosis and induced cell apoptosis by suppressing the activation of SRC.