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Schisanhenol ameliorates oxLDL‐caused endothelial dysfunction by inhibiting LOX‐1 signaling
Atherosclerotic lesions play a critical role in leading cardiovascular diseases. Oxidized low‐density lipoprotein (OxLDL) is a vital risk factor for atherosclerosis since it acts a crucial role in endothelial dysfunction and foam cell formation. Schisanhenol, a composition extracted from the fruit of Schisandra rubriflora, has been reported to have antioxidative effects on human LDL oxidation. This study investigates whether Schisanhenol protects against oxLDL‐mediated endothelial damage by modulating the lectin‐like oxLDL receptor‐1 (LOX‐1)‐mediated inflammatory processes. Human umbilical vein endothelial cells (HUVECs) were pre‐treated with 10 or 20 μM Schisanhenol for 2 h and then exposed to 150 μg/mL oxLDL. We revealed that Schisanhenol reduced oxLDL‐enhanced LOX‐1 expression. We also found that oxLDL down‐regulated endothelial nitric oxide synthase (eNOS) as well as activated inducible NOS (iNOS), thereby enhancing the generation of nitric oxide (NO). Moreover, oxLDL elevated the expression levels of phosphorylated‐p38MAPK, subsequently promoting NF‐κB‐modulated inflammatory responses. Pretreatment with Schisanhenol exerted significant cytoprotective function in all the above‐mentioned detrimental events. Results from this present study reveal that Schisanhenol has a potential therapeutic effect on preventing oxLDL‐induced endothelial injuries.
Schisanhenol ameliorates oxLDL‐caused endothelial dysfunction by inhibiting LOX‐1 signaling
Atherosclerotic lesions play a critical role in leading cardiovascular diseases. Oxidized low‐density lipoprotein (OxLDL) is a vital risk factor for atherosclerosis since it acts a crucial role in endothelial dysfunction and foam cell formation. Schisanhenol, a composition extracted from the fruit of Schisandra rubriflora, has been reported to have antioxidative effects on human LDL oxidation. This study investigates whether Schisanhenol protects against oxLDL‐mediated endothelial damage by modulating the lectin‐like oxLDL receptor‐1 (LOX‐1)‐mediated inflammatory processes. Human umbilical vein endothelial cells (HUVECs) were pre‐treated with 10 or 20 μM Schisanhenol for 2 h and then exposed to 150 μg/mL oxLDL. We revealed that Schisanhenol reduced oxLDL‐enhanced LOX‐1 expression. We also found that oxLDL down‐regulated endothelial nitric oxide synthase (eNOS) as well as activated inducible NOS (iNOS), thereby enhancing the generation of nitric oxide (NO). Moreover, oxLDL elevated the expression levels of phosphorylated‐p38MAPK, subsequently promoting NF‐κB‐modulated inflammatory responses. Pretreatment with Schisanhenol exerted significant cytoprotective function in all the above‐mentioned detrimental events. Results from this present study reveal that Schisanhenol has a potential therapeutic effect on preventing oxLDL‐induced endothelial injuries.
Schisanhenol ameliorates oxLDL‐caused endothelial dysfunction by inhibiting LOX‐1 signaling
Chiu, Tsan‐Hung (Autor:in) / Ku, Chang‐Wen (Autor:in) / Ho, Tsung‐Jung (Autor:in) / Tsai, Kun‐Ling (Autor:in) / Yang, Yi‐Dung (Autor:in) / Ou, Hsiu‐Chung (Autor:in) / Chen, Hsiu‐I (Autor:in)
Environmental Toxicology ; 38 ; 1589-1596
01.07.2023
8 pages
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
anti‐inflammation , HUVECs , LOX‐1 , oxLDL , Schisanhenol
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