目的:研究白杨素(chrysin)对离体大鼠主动脉肌源性反应的影响,并探讨其作用机制。方法:分离SD大鼠主动脉,采用离体血管环灌流装置观察chrysin对血管环的基础张力及对60 mmol/L KCl预收缩血管的舒张作用,并结合不同抑制剂处理,探讨其作用于血管环的可能机制。结果:Chrysin(10~(-6)mol/L、3×10~(-6)mol/L、10~(-5)mol/L、3×10~(-5)mol/L和10~(-4)mol/L)对基础状态血管无明显影响,但对60 mmol/L KCl预收缩的血管环具有浓度依赖性舒张作用,并且去内皮组舒张作用弱于内皮完整组(P〈0.05)。NOS抑制剂L-NAME(10~(-4)mol/L)处理血管后,chrysin的舒张血管作用部分被抑制(P〈0.05),COX抑制剂吲哚美辛(10~(-5)mol/L)处理血管后无明显抑制作用。钾通道阻滞剂4-氨基吡啶(10~(-3)mol/L)、氯化钡(10~(-4)mol/L)、格列苯脲(10~(-5)mol/L)和四乙胺(10^-3mol/L)预孵后,chrysin舒张血管作用均被部分抑制(P〈0.05)。Chrysin(10~(-6)mol/L、10~(-5)mol/L和10~(-4)mol/L)可浓度依赖性抑制2.5 mmol/L Ca Cl_2引起的主动脉收缩。结论:Chrysin能够浓度依赖性舒张大鼠主动脉,其作用机制可能与促进一氧化氮释放、激活4种K^+通道及减少细胞内钙离子浓度有关。
AIM: To determine the effect of chrysin on the relaxation of isolated rat aortic rings and its mechanisms. METHODS: On ex vivo aortic ring perfusion device,the influence of chrysin on isolated aortic ring at basic condition or contraction of the aorta induced by KCl( 60 mmol / L) was observed,and the effects of chrysin on the blood vessel reaction induced by various drugs were recorded. RESULTS: Chrysin( 10~(- 6)mol / L,3 × 10~(- 6)mol / L,10~(- 5)mol / L,3 ×10~(- 5)mol / L and 10~(- 4)mol / L) had no effect on isolated aortic ring at basic condition. Chrysin had stronger vasodilatation effect in intact group than that in non-intact group( P 0. 05). Treatment of the arterial rings with e NOS inhibitor LNAME,but not with indomethecin or endothelium denudation,obviously affected the relaxant effects of chrysin( P 0. 05). When the contractions were induced by KCl,4-aminopyridine( 10~(- 3)mol / L),Ba Cl_2( 10~(- 4)mol / L),glibenclamide( 10~(- 5)mol / L),and tetraethylammonium( 10~(- 3)mol / L) weakened chrysin-induced diastolic effect( P 0. 05). Chrysin significantly inhibited contracting effect of KCl on aorta rings in 2. 5 mmol / L Ca~(2 +)medium( P 0. 05). CONCLUSION:Chrysin exerts vasodilating effect on rat isolated aorta rings in a dose-dependent manner. The mechanism might be related to promoting NO release,activating K~+channels and decreasing the concentration of cytoplasmic Ca~(2 +).