Prevention of hypertension, cardiovascular damage and endothelial dysfunction with green tea extracts
Prevention of hypertension, cardiovascular damage and endothelial dysfunction with green tea extracts
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DOI：
10.1016/j.amjhyper.2007.08.006
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发表时间：
2007-12-01
影响因子：
3.2
通讯作者：
Rossi, Gian Paolo
中科院分区：
文献类型：
--
作者：
Antonello, Michele;Montemurro, Domenico;Rossi, Gian Paolo
背景：我们研究了绿茶提取物(GTE)对高氧化应激的动脉高压的影响。血管紧张素(Ang)II诱导血管内皮细胞功能障碍是动脉粥样硬化和高血压的关键因素。方法：13周龄雄性SD大鼠，随机分为饮用GTE(6 mg/m L)和饮用GTE(6 mg/m L)两组，分别给予高剂量(700 mU/kg/d)和低剂量(350 mU g/kg/d)Ang II，共13天。用遥测法测量血压。处死后测定左心室重量指数、肠系膜小动脉中腔比和苯肾上腺素预收缩动脉对乙酰胆碱的浓度-反应曲线。观察超氧化物歧化酶(SOD-1)类似物坦普尔对乙酰胆碱所致动脉反应的影响。氧化应激通过血浆过氧化氢和硝基酪氨酸水平进行测定。结果：与载体组比较，AngⅡ组大鼠的血压、左心室重量指数、中腔比和氢过氧化氢自由基均明显升高。GTE抑制了这些增加，阻止了Ang II引起的主动脉HO-1、p22(Phox)和SOD-1mRNA的增加，并将其降低到基线水平以下。低剂量血管紧张素转换酶II仅在第一周升高血压和血浆过氧化氢。两个Ang II剂量均使曲线右移至乙酰胆碱；GTE在体内可阻止这一作用，体外可被Templ所消除。结论：GTE可预防大剂量Ang II所致的高血压和靶器官损伤，其机制可能与防止或清除超氧阴离子的产生有关。Am J Hyperten 2007；20：1321-1328(C)2007美国高血压杂志。
Background: We investigated the effect of green tea extract (GTE) in arterial hypertension with high oxidative stress. Angiotensin (Ang) II induces endothelial dysfunction (ED) that is crucial for the development of atherosclerosis and hypertension.Methods: Male Sprague-Dawley rats, 13 weeks old, randomly assigned to drinking water with or without GTE (6 mg/mL) received a vehicle, a high (700 mu g/kg/d) or a low (350 mu g/kg/d) Ang II dose for 13 days, by osmotic mini-pumps. Blood pressure (BP) was measured with telemetry. After sacrifice, left ventricular (LV) mass index, small mesenteric artery media-to-lumen ratio, and concentration-response curves of phenylephrine-precontracted arteries to acetylcholine were evaluated. The effect of the superoxide dismutase (SOD-1) analog tempol on artery responses to acetylcholine was assessed. Oxidative stress was measured by plasma hydroperoxides and nitrotyrosine levels. The mRNA of heme oxygenase 1 (HO-1), NADPH oxidase endothelial p22(phox) subunit, and SOD-1 was also measured in the aorta.Results: Compared with vehicle high Ang II increased BP, LV mass index, media-to-lumen ratio, and hydroperoxide radicals. The GTE blunted these increases, prevented the increase in HO-1, p22(phox), and SOD-1 mRNA in aorta caused by Ang II, and reduced them below baseline levels. Low Ang II dose increased BP values and plasma hydroperoxides only during the first week. Both Ang II doses shifted rightward the curves to acetylcholine; this was prevented in vivo by GTE and abolished in vitro by tempol.Conclusions: The GTE prevented hypertension and target organ damage induced by a high Ang II dose, likely by prevention or scavenging of superoxide anion generation. Am J Hypertens 2007;20:1321-1328 (c) 2007 American Journal of Hypertension, Ltd.