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• W2898569576 abstract "Osthole, a naturally-derived coumarin, has been shown to exhibit pharmacological activities including anti-inflammatory, anti-oxidative and cardiovascular protective effects. However, the effect of osthole on oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury and its underlying mechanism remain unknown. We found that osthole did not affect viability of human umbilical vein endothelial cells (HUVECs) but alleviated ox-LDL-induced cytotoxicity in HUVECs. Osthole repressed ox-LDL-induced release of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 in HUVECs. Osthole reversed ox-LDL-induced elevation of reactive oxygen species (ROS) production and malondialdehyde (MDA) level, and reduction of superoxide dismutase (SOD) activity in HUVECs. Meanwhile, osthole attenuated ox-LDL-induced increase of mRNA expression and secretion of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs. Osthole increased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) phosphorylation in ox-LDL-treated HUVECs. Furthermore, osthole inhibited ox-LDL-induced activation of the transforming growth factor-β1 (TGF-β1)/Smad pathway and activation of TGF-β1/Smad pathway by TGF-β1 attenuated the protective effects of osthole on HUVECs injury. These results suggested that osthole attenuated ox-LDL-induced HUVECs injury by inhibiting the TGF-β1/Smad pathway, suggesting that osthole might be a promising therapeutic agent for the treatment of atherosclerosis." @default.
• W2898569576 created "2018-11-02" @default.
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• W2898569576 date "2018-12-01" @default.
• W2898569576 modified "2023-09-26" @default.
• W2898569576 title "Osthole alleviates oxidized low-density lipoprotein-induced vascular endothelial injury through suppression of transforming growth factor-β1/Smad pathway" @default.
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• W2898569576 doi "https://doi.org/10.1016/j.intimp.2018.10.031" @default.
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