Salvianolic acid B attenuates oxidized low-density lipoprotein-induced endothelial cell apoptosis through inhibition of oxidative stress, p53, and caspase-3 pathways.

OBJECTIVE

To investigate the effect of salvianolic acid B (Sal B) on oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) apoptosis and the possible mechanism.

METHODS

HUVECs were divided into 6 groups, including control group, ox-LDL group, vitamin C group (positive control), and 5, 10 and 20 μg/mL Sal B groups. Cell viability of HUVECs was determined by 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The anti-apoptotic effect of Sal B was tested by Hoechst 33258 staining and Annexin V/propidium iodide flflow cytometry analysis. Apoptosis-related genes (p53, Bcl-2 and Bax) expression and caspase-3 activity were also determined. Oxidative stress markers malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by the corresponding kits.

RESULTS

In HUVECs, ox-LDL signifificantly reduced cell viability and induced apoptosis (P<0.05 or P<0.01), however, Sal B diminished the effects of ox-LDL in a dose-dependent manner (P<0.05). Moreover, 10 and 20 μg/mL Sal B reduced the expression levels of p53, increased the Bcl-2/Bax ratio and inhibited the caspase-3 activity in ox-LDL-treated HUVECs (P<0.05). In addition, 5, 10 and 20 μg/mL Sal B signifificantly enhanced the activity of SOD, while decreased the level of MDA in the HUVECs which treated with ox-LDL (P<0.05).

CONCLUSION

Sal B exhibited anti-apoptotic effects in ox-LDL-induced endothelial cell injury by suppressing oxidative stress, p53, and caspase-3.