Schisanhenol attenuated ox-LDL-induced apoptosis and reactive oxygen species generation in bovine aorta endothelial cells in vitro.

The aim of this paper was to investigate the protective effect of schisanhenol (Sal) isolated from Schisandra rubriflora Rhed, on human ox-LDL-induced bovine aorta endothelial cells (BAECs) apoptosis and intracellular reactive oxygen species (ROS) production in vitro. The BAECs were cultured with ox-LDL (200 microg/ml) in the presence and absence of Sal (10 and 50 micromol L(- 1)) for 24 h. The cytotoxicity of ox-LDL was evaluated by LDH leakage, cell viability and morphological change. Cell apoptosis was estimated by DNA ladder, chromatin condensation, and flow cytometry assay. The intracellular ROS production was detected by using DCF, a ROS probe, with laser confocal microscopy and flow cytometry. Sal was shown to reduce LDH leakage and increase cell viability. Sal also attenuated ox-LDL-induced BAECs apoptosis as indicated in typical internucleosomal DNA degradation (DNA ladder), condensed chromatin, and the sub-G1 peak appearance in flow cytometry assay. Furthermore, Sal was shown to inhibit ROS generation in BAECs with stimulation of ox-LDL. The results indicated that the anti-apoptosis effect of Sal on BACSs might be related to its inhibition of ROS generation.