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作 者:张海宁[1] 张涵[1] 柳玉梅[1] 赖世龙[1] 陈海琪 张根水[1] 张贵平[1]
出 处:《中药药理与临床》2015年第1期37-40,共4页Pharmacology and Clinics of Chinese Materia Medica
基 金:广州市教育局基金资助项目(No:10A179)
摘 要:目的:考察红景天苷舒张血管的作用及机制,分析其可能的作用靶点。方法:取同批大鼠胸主动脉制成离体血管环,通过记录血管环的张力变化,观察给予不同处理时,红景天苷对血管环舒缩作用的影响。结果:红景天苷(10-11mol/L^10-5mol/L)可内皮依赖性地舒张血管;0.01mmol/L吲哚美辛(Indomethacin)可使红景天苷的量效曲线下降趋势明显减弱,而0.1mmol/L亚硝基左旋精氨酸甲酯(L-NAME)则无明显影响;0.1mmol/L Ba Cl2也不影响红景天苷的舒张血管作用;10-6mol/L和10-5mol/L红景天苷可减缓无钙高钾环境下Ca2+收缩曲线的上升趋势,并可抑制无钙液中PE引起的缩血管作用。结论:红景天苷对胸主动脉血管的舒张作用具有内皮依赖性,并与内皮产生的前列环素有关,与NO-CGP通路无关。而红景天苷对VDCC和ROCC介导的胞内钙升高的直接调节则可能介导了其内皮非依赖性的血管舒张作用。Objective: To investigate the vasodilatory effect of salidroside on the thoracic aortic ring isolated from SD rats. Methods: The aortic rings with or without the endothelium were pretreated with different reagents,and the isometric tension of aortic rings was recorded before and after preconstricted by phenylephrine( PE). The changes of tension reflected the vasodilatory effect of salidroside. Results: Salidroside( 10^-11 mol / L ~ 10-^5mol / L) endothelium-dependently relaxed the aortic rings pre-contracted by PE in a concentration-dependent manner. This effect was significantly reduced by pretreatment of indomethacin( 0. 01 mmol / L),but not by 0. 1mmol / L of L-N( w)-nitro-arginine methyl ester( L-NAME). Pretreatment of aortic ring with Ba Cl2( 0. 1mmol/L) also did not affect the vasodilatory effect of salidroside. On the other hand,The salidroside( 10^-6mol / L,10-^5mol / L) incubation attenuated potassium-stimulated Ca2 +-dependent contraction due to Ca2 +influx and inhibited the Ca2 +-dependent contraction due to Ca2 +release from ER induced by PE in calcium-free buffer. Conclusion: All these results suggested that the vasodilatory effect of salidroside on the aortic ring was endothelium-dependent. The COX-PGI2 signaling pathway,but not NO-c GMP signaling pathway,may be involved in the endothelium-dependent relaxation of salidroside. While,the inhibition of salidroside on Ca2 +-dependent contraction due to Ca2 +influx via VDCC or Ca2 +release via ROCC contributed to its endothelium-independent relaxation on the aortic ring.
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