Key result
Qiliqiangxin prevents oxidized low-density lipoprotein-induced injury in human coronary artery endothelial cells by decreasing apoptosis via reduction of caspase-3 activity.
Why the study?
Does Qiliqiangxin prevent oxidized LDL-induced injury in human coronary artery endothelial cells?
Does Qiliqiangxin prevent oxidized LDL-induced injury in human coronary artery endothelial cells?
p-value: p=<0.05
Qiliqiangxin protects human coronary artery endothelial cells from oxLDL-induced injury by reducing apoptosis via caspase-3 activity.
Qiliqiangxin (QL) has protective effect for the cardiovascular diseases treatment.This study aim to evaluate the effect of QL on the cell viability, cell apoptosis and caspase-3 activity in oxidized LDL (oxLDL)-induced Human Coronary Artery Endothelial Cells (HCAECs).HCAECs were treated with QL (0-1µg/ml) and oxLDL (150 μg/ml).The HCAECs viability was detected by cell proliferation assay and Lactate Dehydrogenase (LDH) release assay.The HCAECs apoptosis was evaluated by the annexin V-FITC assay.The activity of caspase-3 of HCAECs was measured by colorimetric caspase-3 assay.Cell migration assay and capillary-like tube formation assay on Matrigel were performed.Treatment of HCAECs to ox-LDL (150 μg/ml) decreased cell viability, stimulated apoptosis and enhanced caspase-3 activity.In addition, treatment with QL (0.5 µg/ml) alone did not affect cell viability and LDH release.Furthermore, the treatment with QL (0.5 µg/ml) significantly increased ox-LDL (150 μg/ml) decreased cell viability.Treatment with QL (0.5 µg/ml) reduced ox-LDL-stimulated apoptosis and caspase-3 activity in HCAECs in a dose-dependent manner.QL (0.5 µg/ml) attenuated ox-LDL (150 μg/ml) abolished cell migration and tube formation.Our study demonstrated that QL prevents ox-LDLinduced HCAECs injury by decreasing the apoptosis via caspase-3 activity.
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Du et al. (2018) studied ox-LDL-induced endothelial cell injury. Qiliqiangxin vs. ox-LDL alone was evaluated on Cell viability and apoptosis (p=<0.05). Qiliqiangxin prevents oxidized low-density lipoprotein-induced injury in human coronary artery endothelial cells by decreasing apoptosis via reduction of caspase-3 activity.
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