羟基红花黄色素A的血管作用及其机制研究  

Vascular effect of hydroxyl-safflor yellow A and underlying mechanism

作　　者：张琳[1] 沈国舜[1] 张镜年[1] 聂培鹤[1] 支建明[1] 

机构地区：[1]上海交通大学基础医学院生理学教研室,上海200025

出　　处：《上海交通大学学报（医学版）》2009年第4期431-434,共4页Journal of Shanghai Jiao tong University:Medical Science

摘　　要：目的探讨羟基红花黄色素A（HSYA）对离体大鼠胸主动脉环收缩功能的影响及其机制。方法采用生物信号采集系统记录灌流大鼠胸主动脉环张力变化，观察HSYA（1×10^-6～1×10^-4mol／L）对苯肾上腺素（PE）（1×10^-6～1×10^-4mol／L）、KCl（6×10^-2mol／L）和CaCl2（1×10^-5～3×10^-3mol／L）收缩血管功能的影响，并观察钌红（RR）或肝素（HP）预处理对HSYA作用的影响。结果HSYA抑制KCl、PE对完整内皮和去内皮血管环的收缩作用，且呈浓度依赖性。HSYA可使CaCl2量-效曲线下移，呈浓度依赖性。HSYA＋HP抑制血管收缩的作用比单用HSYA明显（P〈0．05），与HP相比差异无统计学意义（P〉0．05）；HSYA＋RR抑制血管收缩的作用与单用RR或HSYA比较，差异均有统计学意义（P〈0．05）。结论HSYA的血管作用可能是通过抑制Ca^2＋内流和减小Ca^2＋浓度实现的。Objective To investigate the vascular effect of hydroxyl-safflor yellow A （HSYA） on rat thoracic aorta and its underlying mechanism. Methods The tension of isolated thoracic aorta rings of rats perfused with different concentrations of HSYA （ 1 ×10^-6～1×10^-4mol/L） was measured using organ bath technique. The effects of HSYA on the vasocontraction induced by cumulative phenylephrine （PE） （ 1×10^-6～1×10^-4 mol/L） , KCl （6 × 10^-2 mol/L） and CaCl2 （1 × 10^-5 - 3 × 10^-3 mol/L） were recorded respectively. Results HSYAcaused a concentration-dependent anticontraction effects by KCl or PE in endothelium-intact and endothelium-denuded aortic rings. HSYA inhibited the CaCl2- induced contraction and downward shifted concentration-response curve of aortic rings. HSYA ＋ HP resulted in more significant anti-contraction effect than single use of HSYA （P 〈 0.05）, while there was no significant difference in that between HSYA ＋ HP and HP（P 〉0.05）. There were significant differences in anti-contraction effect between HSYA ＋ RR and RR or HSYA（P 〈 0.05）. Conclusion The role of HSYA may be mediated by reducing Ca^2＋ influx and Ca^2＋ concentration.

关 键 词：羟基红花黄色素A 血管收缩 RYANODINE受体 1 4 5-三磷酸肌醇受体 

分 类 号：R285.5[医药卫生—中药学]