Department of Human Nutrition, Foods and Exercise, College of Agriculture and Life Sciences, Virginia Tech, Blacksburg, VA, 24061, USA.
Eur J Nutr. 2014 Feb;53(1):269-75. doi: 10.1007/s00394-013-0525-7. Epub 2013 Apr 21.
Luteolin, a flavone present in many foods and medicinal plants, may have beneficial effects on various human chronic diseases. In the present study, we investigated the hypothesis that luteolin can directly act on vascular endothelial cells (ECs), leading to nitric oxide (NO) production and subsequent vascular relaxation.
Rat aortic rings were mounted in organ bath. Luteolin was added cumulatively, and vessel relaxation of rat aortic rings precontracted with phenylephrine (PE) or potassium was recorded. Endothelial nitric oxide synthase (eNOS) phosphorylation at Ser1177 and NO production from aortic rings and primary human aortic endothelial cells (HAECs) exposed to luteolin were measured by using Western blot and fluorometric assay, respectively.
Luteolin dose-dependently (10-100 μmol/L) elicited relaxation of PE- or potassium-contracted aortic rings. The vasorelaxation effect of luteolin was attenuated by the eNOS inhibitor, N-nitro-L-arginine methyl ester, suggesting that this luteolin action is at least partially mediated by activating eNOS activity. We further found that luteolin dose-dependently (10-100 μmol/L) increased eNOS phosphorylation at Ser1177 (up to 1.9-fold) in isolated rat rings. Consistently, exposure of HAECs to luteolin also increased eNOS phosphorylation and NO production.
Luteolin may be a vascular protective agent by directly acting on vascular ECs to stimulate NO-dependent vascular dilatation.
木犀草素是一种存在于许多食物和药用植物中的类黄酮，可能对各种人类慢性疾病有有益的影响。在本研究中，我们假设木犀草素可以直接作用于血管内皮细胞（EC），导致一氧化氮（NO）的产生和随后的血管舒张。
将大鼠主动脉环安装在器官浴中。累积添加木犀草素，并记录预先用苯肾上腺素（PE）或钾收缩的大鼠主动脉环的血管舒张。通过Western blot 和荧光测定分别测量暴露于木犀草素的主动脉环和原代人主动脉内皮细胞（HAEC）中内皮型一氧化氮合酶（eNOS）丝氨酸 1177 磷酸化和 NO 的产生。
木犀草素（10-100μmol/L）剂量依赖性地引起 PE 或钾收缩的主动脉环舒张。eNOS 抑制剂 N-硝基-L-精氨酸甲酯削弱了木犀草素的血管舒张作用，表明这种木犀草素作用至少部分是通过激活 eNOS 活性介导的。我们进一步发现，木犀草素（10-100μmol/L）剂量依赖性地增加了分离的大鼠环中 eNOS 丝氨酸 1177 的磷酸化（增加了 1.9 倍）。一致地，HAEC 暴露于木犀草素也增加了 eNOS 磷酸化和 NO 的产生。
木犀草素可能通过直接作用于血管内皮细胞来刺激依赖 NO 的血管扩张，从而成为一种血管保护剂。
