Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan.
J Agric Food Chem. 2009 Dec 9;57(23):11406-17. doi: 10.1021/jf902876p.
Sesamin, a lignan from sesame oil, has been shown to have antihypertensive and antioxidative properties. This study examined the effects of sesamin on oxidized low-density lipoprotein (oxLDL)-induced endothelial dysfunction. Oxidative stress was determined by measuring the generation of intracellular reactive oxygen species (ROS) and by measuring the expression levels of superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS). To assess the pro-inflammatory effects of oxLDL, ELISA was used to detect IL-8 expression, endothelin-1 (ET-1) secretion, and nuclear factor-kappaB (NF-kappaB) activation. The expression of adhesion molecules (ICAM-1, VCAM-1, and E-selectin) was examined by flow cytometry. In addition, several apoptotic signaling pathways were also investigated. The data showed that sesamin significantly ameliorated oxLDL-induced ROS generation and SOD-1 inactivation. Sesamin also attenuated the oxLDL-induced activation of NF-kappaB, suggesting that the inhibitory effects of sesamin on IL-8 and ET-1 release, adhesion molecule expression, and the adherence of THP-1 cells were at least partially through the blockade of NF-kappaB activation. Furthermore, sesamin attenuated oxLDL-induced apoptotic features, such as intracellular calcium accumulation and the subsequent collapse of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-3. Results from this study may provide insight into possible molecular mechanisms underlying sesamin's beneficial effects against oxLDL-mediated vascular endothelial dysfunction.
芝麻素是芝麻油中的一种木脂素,具有降血压和抗氧化作用。本研究探讨了芝麻素对氧化型低密度脂蛋白(oxLDL)诱导的血管内皮功能障碍的影响。通过测量细胞内活性氧(ROS)的生成和超氧化物歧化酶(SOD)和内皮型一氧化氮合酶(eNOS)的表达水平来确定氧化应激。为了评估 oxLDL 的促炎作用,通过 ELISA 检测白细胞介素-8(IL-8)表达、内皮素-1(ET-1)分泌和核因子-κB(NF-κB)激活。通过流式细胞术检测粘附分子(ICAM-1、VCAM-1 和 E-选择素)的表达。此外,还研究了几种凋亡信号通路。结果表明,芝麻素可显著改善 oxLDL 诱导的 ROS 生成和 SOD-1 失活。芝麻素还减弱了 oxLDL 诱导的 NF-κB 激活,表明芝麻素对 IL-8 和 ET-1 释放、粘附分子表达和 THP-1 细胞黏附的抑制作用至少部分是通过阻断 NF-κB 激活来实现的。此外,芝麻素减弱了 oxLDL 诱导的凋亡特征,如细胞内钙积累和随后的线粒体膜电位崩溃、细胞色素 c 释放和 caspase-3 激活。本研究的结果可能为芝麻素对 oxLDL 介导的血管内皮功能障碍的有益作用提供潜在的分子机制。