血管紧张素Ⅱ对急性缺氧时血管内皮细胞分泌内皮素的影响及茶多酚的保护作用研究

目的观察急性缺氧条件下,血管紧张素Ⅱ（AngⅡ）对血管内皮细胞（VEC）分泌内皮素（ET）的影响及茶多酚（TP）的保护作用。方法将培养的VEC分为7个组：①空白对照组;②单纯缺氧组;③缺氧＋TP组;④单纯AngⅡ组;⑤AngⅡ＋TP组;⑥缺氧＋AngⅡ组;⑦缺氧＋AngⅡ＋TP组。除空白对照组、单纯AngⅡ组和AngⅡ＋TP组外,其他各组置于低压舱内上升至5000M高度、停留30min,对培养的各组VEC进行缺氧。用放射免疫法测定缺氧及AngⅡ和TP作用前、作用后0.5h、6h、24h不同时间点各组细胞培养液中的ET含量。结果①急性缺氧和单纯AngⅡ均可明显促进VEC分泌ET（P〈0.01）,在急性缺氧条件下,AngⅡ促进VEC分泌ET的作用要显著高于单纯缺氧作用和单纯AngⅡ作用（P〈0.01）。②TP能显著降低缺氧及AngⅡ促VEC分泌ET的作用（P〈0.01）。结论在急性缺氧条件下,AngⅡ可显著增加培养的VEC分泌ET的功能,TP能显著抑制缺氧条件下AngⅡ促VEC分泌ET的作用。

Effect of Angiotensin Ⅱ and Tea Polyphenols on ET Secretion in VEC Induced by Hypoxia

Objective To explore the effect of angiotesin Ⅱ （AngⅡ） on vascular endothelial cells （VEC） secreting endothelin （ET） induced by hypoxia and study the protective effect of tea polyphenols （TP）.Methods Cultured VEC were divided into 7 groups： control group, simple hypoxia group, hypoxia＋TP group, simple AngⅡ group, AngⅡ＋TP group, hypoxia＋AngⅡ group and hypoxia＋AngⅡ＋TP group. Hypoxia group, hypoxia＋TP group, hypoxia＋AngⅡ group and hypoxia＋AngⅡ＋TP group underwent hypoxia in hypobaric chamber imitating the conditions 5000 meters above sea level for 30 min. ET content in supernatant of VEC culture before hypoxia and 0.5 h, 6 h, 24 h after hypoxia were measured with radioimmunoassay.Results Simple hypoxia or simple AngⅡ promoted VEC to secrete ET significantly （P〈0.01）; AngⅡ increased ET release of VEC induced by hypoxia, the effect of which was significantly stronger than simple hypoxia or simple AngⅡ （P〈0.01）. TP could significantly inhibit ET secretion from VEC induced by hypoxia and AngⅡ （P〈0.01）.Conclusion AngⅡ can significantly increase ET release of VEC induced by hypoxia, while TP can eliminate such effect.