3,4-DI-O-CAFFEOYL QUINIC ACID保護血管內皮細胞對抗氧化性損傷及修復內膜依賴性血管舒張反應

3,4-Di-O-Caffeoyl Quinic Acid Protects Endothelial Cells Against Oxidative Stress and Restores Endothelium-Dependent Vasodilatation

本文研究地膽草（Elephantopus mollis H. B. K.） 酚類成份3,4-di-O-caffeoyl quinic acid 對於氧化壓力所造成血管內皮細胞損傷的保護作用。結果顯示3,4-di-O-caffeoyl quinic acid （1 to30 μM）可清除DPPH自由基、且活性大於resveratrol。由TBARS的實驗發現3,4-di-O-caffeoylquinic acid也可有效抑制Fenton's reagent （H2O2/FeSO4） 引起的細胞膜氧化損傷。此外，3,4-di-Ocaffeoylquinic acid不但可以減低Fenton's reagent （H2O2/FeSO4）所造成的人類臍靜脈血管內皮細胞（human umbilical vein endothelial cells, HUVEC） 死亡，也可以使胸主動脈血管遭破壞的內膜依賴性舒張反應得以恢復。以上結果顯示3,4-di-O-caffeoyl quinic acid 可對抗氧化性損傷，而自由基清除作用可能就是此成份的細胞保護機轉之一。We investigated the cytoprotective effect of 3,4-di-O-caffeoyl quinic acid, a phenolic compound isolated from Elephantopus mollis H. B. K. (Compositae), on oxidative stress-induced cell damage in vascular endothelial cells. Result showed that 3,4-di-O-caffeoyl quinic acid (1 to 30 μM) displayed potent DPPH radical scavenger activity more efficient than resveratrol. Free radical-mediated oxidative modification of cell membrane by Fenton's reagent (H2O2/FeSO4) was also significantly attenuated by 3,4-di-O-caffeoyl quinic acid as measured by thiobarbituric acid-reactive substances (TBARS). Furthermore, this compound not only effectively minimized the loss of cell viability induced by Fenton's reagent in cultured human umbilical vein endothelial cells (HUVEC) but also significantly reversed H2O2/FeSO4-induced impairment of endothelium-dependent relaxation to acetylcholine in rat aorta. These data suggested that 3,4-di-O-caffeoyl quinic acid prevents cell from oxidative stress and that scavenges of free radical could be key mechanism contribute to the cytoprotective effect of 3,4-di-O-caffeoyl quinic acid.