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羟基红花黄色素A的血管作用及其机制研究 被引量:25

Vascular effect of hydroxyl-safflor yellow A and underlying mechanism
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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.
出处 《上海交通大学学报(医学版)》 CAS CSCD 北大核心 2009年第4期431-434,共4页 Journal of Shanghai Jiao tong University:Medical Science
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 hydroxyl-safflor yellow A vasocontraction ryanodine receptor 1,4,5-trisphophate receptor
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