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目的:研究西红花酸(crocetin,CCT)血管舒张作用及其可能机制。方法:采用RM6240C型多道生物信号采集处理系统,记录灌流大鼠胸主动脉环张力变化。结果:CCT(10-9~10-4mol/L)对苯肾上腺素(PE,10-5mol/L)预收缩的内皮完整血管环产生浓度依赖性的舒张作用;CCT(3×10-9~10-4mol/L)对苯肾上腺素(PE,10-5mol/L)预收缩的去内皮血管环产生浓度依赖性的舒张作用,但内皮完整组血管舒张作用比去内皮组更明显,两者相比,在10-8~10-4mol/L时,具有显著性差异(P<0.01)。CCT对高浓度KCl(6×10-2mol/L)预收缩的血管环无明显的舒张作用。一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(10-4mol/L)或前列环素合成酶抑制剂吲哚美辛(10-5mol/L)预处理,对CCT诱导的内皮完整动脉环舒张作用具有明显的抑制效应。ATP敏感性K+通道阻断剂格列苯脲(3×10-6mol/L)预处理后,CCT的舒血管作用均无显著变化(P>0.05),但Ca2+激活K+通道抑制剂四乙胺(5×10-3mol/L)或电压敏感性K+通道抑制剂4-氨基吡啶(10-3mol/L)预处理,可明显减弱CCT引起的无内皮血管舒张作用(P<0.01)。结论:CCT对大鼠胸主动脉具有部分内皮依赖性舒张作用,其内皮依赖性血管舒张作用的机制,与其促进内皮一氧化氮合酶或环氧合酶途径,从而增加一氧化氮和前列环素的生成有关;其内皮非依赖性舒血管效应的作用机制涉及Ca2+激活K+通道或电压敏感型K+通道的激活。
Objective: To investigate the vasodilation effect of crocetin (CCT) and its possible mechanism. Methods: Multi-channel biological signal acquisition and processing system RM6240C was used to record the changes of thoracic aortic ring tension in perfusion rats. Results: CCT (10-9 ~ 10-4mol / L) produced a concentration-dependent relaxation effect on pre-contracted endothelial angiogenesis of phenylephrine (PE, 10-5mol / L) 10 -4 mol / L) produced a concentration-dependent relaxation of the pre-contracted endothelium-vascular rings of phenylephrine (PE, 10-5 mol / L), but the vasodilation of the intact endothelium group was more pronounced than that of the endothelium- Compared with 10-8 ~ 10-4mol / L, there was a significant difference (P <0.01). CCT had no obvious relaxation effect on the precontracted vascular rings of KCl (6 × 10-2mol / L). Nitric oxide synthase inhibitor L-NOS (10-4mol / L) or prostacyclin synthase inhibitor indomethacin (10-5mol / L) pretreatment, CCT-induced endothelial integrity Diastolic arterial ring has a significant inhibitory effect. There was no significant change in the vasodilatation of CCT after ATP-sensitive K + channel blocker glibenclamide (3 × 10-6mol / L) pretreatment, but Ca2 + -activated K + channel inhibitor tetraethylamine (5 × 10-3mol / L) or K (superscript +) channel inhibitor 4-aminopyridine (10-3mol / L) preconditioning could significantly reduce the effect of CCT on endothelial vasodilation (P <0.01). CONCLUSION: CCT has a part of endothelium-dependent relaxation in the thoracic aorta of rats, and its mechanism of endothelium-dependent vasodilation may be related to the promotion of endothelial nitric oxide synthase or cyclooxygenase pathway, thereby increasing nitric oxide and prostacyclin The mechanism by which the endothelium-independent vasodilator effect involves the activation of Ca2 + -activated K + channels or voltage-sensitive K + channels.