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Vascular Calcification, an important risk factor of coronary heart disease (CHD), causes plenty of cardiovascular events. However, no clinical therapies exist to treat or prevent it. Previous researches have suggested that oxidative stress can accelerate vascular calcification. The potential link between osthole, an oxidative inhibitor, and vascular calcifition has not been proved.
ApoE / mice were fed with high fat diet (HFD) and water with or without 20μmol/ml osthole for 8 weeks. Age-matched ApoE /- mice were used as controls (CON). Metabolic parameters, tissue nonspecific alkaline phosphatase (TNAP) activity, aortic calcium content, malondialdehyde (MDA) content, Cu/Zn superoxide dimutase (SOD) activity were measured. In vitro, vascular smooth muscle cells (VSMCs) were cultured with DMEM containing 10 μmol/ml ß-glycerophosphate (ß-GP) and 25 μmol/ml oxidized low-density lipoprotein (ox-LDL) in Cal group. Osthole group was additionally added with 20μmol/ml osthole for 24h. Calcium content and TNAP activity were measured to identify osteoblastic differentiation and mineralization. The expression of Cu/Zn SOD and NADPH oxidase Nox1 were examined with Western blots.
The osthole group showed a significant reduction in TNAP activity, calcium content, MDA content, while Cu/Zn SOD activity increased significantly. In vitro, the level of NOX1, calcium content and TNAP activity were significantly higher in Cal group compared with Osthole group, though expression of Cu/Zn SOD was observably lower.
Osthole decreases vascular calcification through inhibition of oxidative stress.