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作 者:李琳[1] 张冬慧[2] 徐培涵[3] 王婷[3] 梁莉[3] 乔华[3] 常威[3] 李丹[3] 李玲[3]
机构地区:[1]兰州大学第一医院检验科,兰州730000 [2]甘肃省人民医院药剂科,兰州730000 [3]兰州大学第一医院药物临床试验机构,兰州730000
出 处:《中药药理与临床》2013年第6期22-25,共4页Pharmacology and Clinics of Chinese Materia Medica
摘 要:目的:研究羟基红花黄色素A(HSYA)对离体猪冠状动脉血管的舒张作用及其可能作用机制,为红花的生物学活性研究和应用提供参考。方法:以猪冠状动脉血管环为材料,以离体血管功能实验方法检测羟基红花黄色素A对猪冠状动脉血管活性作用。结果:羟基红花黄色素A对静息状态猪冠状动脉血管环无明显舒张作用;HSYA在10^-4.5~10^-2mol/L的浓度范围内对PGFh(10^-6mol/L)预收缩的冠状动脉血管环具有浓度依赖性舒张作用,最大舒张效应为124.22%±6.25%,相应的pD2值为2.91±0.23,HSYA的有效剂量为10^-3mol/L,该剂量能使PGF2α(10^-6mol/L)预收缩的冠状动脉血管环达到65.55%±4.15%的舒张效应;HSYA可使KCl的量效曲线下移,呈浓度依赖性。用一氧化氮合成酶抑制剂L—NNA、鸟苷酸环化酶抑制剂亚甲蓝、β受体阻断剂普萘洛尔、β1受体抑制剂atenolol和B2受体抑制剂ICI 118551预处理后,均可明显减弱HSYA诱导的舒张血管作用;前列腺素合成酶抑制剂吲哚美辛,K+通道抑制剂TEA预处理后,血管舒张作用不能被阻断。结论:羟基红花黄色素A的舒血管活性作用通过内皮.NO.cGMP途径和β-肾上腺素受体途径,并能够阻断血管平滑肌上的电压依赖性钙通道,但与血管平滑肌舒张因子前列腺素的释放及钾离子(KCa)通道无关。Objective:Through the study of hydroxysaftlor yellow A on isolated porcine coronary artery vascular vasodilation function and its possible mechanism of action, as the study of biological activity and application of safflower reference. Methods:The materials was porcine coronary arterial rings, in vitro vascular function detection of hydroxysafflor yellow A vasoaetive effects. Results:HSYA did not change the resting tension of porcine coronary arterial ring; but HSYA in 10^-4.5 - 10^2 mol/L concentration range showed concentration-dependent relaxant effects with PGF2α ( 10^-6 mol/L) -pre-contracted coronary arteries,the two values were 124.22%± 6.25% (Emax) and 2.91 ±0.23( pD2 ). The effective dose of HSYA is 10^-3 mol/L, The dose can make PGF2α(10^-6 mol/L)-pre-contracted coronary arteries get to 65.55% ±4.15% relaxation effect. HSYA inhibited the KCl-induced contraction and downward shifted concentration-response curve of coronary artery rings. Incubation with L-NNA( an inhibitor of NOS), methylene blue( an inhibitor of cGMP synthesis), propranolol( β-adrenoceptor antagonist) , β1 -adrenoceptor antagonist atenolol,as well as β2-adrenoceptor antagonist ICI 118551 significantly attenuated the vaso-relaxation in porcine coronary rings induced by HSYA. However, incubation with indomethacin ( an inhibitor of COX), tetraethylammonium ( an inhibitor of K * channels) did not affect the vaso-relaxation. Conclusion:The effect of HSYA on vasodilator may relate to activation of β2-adrenoceptors, dependent VDCC, and endothelium-NO-cGMP pathway,but not related to PGI2 pathway and potassium channels.
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