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目的:探讨染料木素(genistein,GST)对对氧磷(paraoxon,PO)损伤血管功能的保护作用。方法:取雄性SD大鼠胸主动脉制备离体血管环,测量并记录血管环张力。实验分组如下:1)溶媒对照组,用0.1%的二甲基亚砜(dimethyl sulfoxide,DMSO)预孵育血管环30 min后,检测大鼠胸主动脉环对乙酰胆碱(acetylcholine,Ach;1×10-9～1×10-5 mol/L)诱导的内皮依赖性舒张(endothelium-dependent relaxation,EDR)功能及硝普钠(sodiumnitroprusside,SN P;1×10-6 mol/L)诱导的非内皮依赖性舒张功能的反应;2)各浓度PO处理组,分别用不同浓度的PO(4.05×10-9～4.05×10-5 mol/L)预孵育血管环30 min后,检测大鼠胸主动脉环对Ach及SN P诱导的血管舒张功能的反应;3)PO+GST处理组,分别用PO(4.05×10-6 mol/L)与不同浓度的GST(1,3,10,30或100μmol/L)共同孵育血管环30 min后,检测大鼠胸主动脉环对Ach及SN P诱导的血管舒张功能的反应及对苯肾上腺素(phenyllphrine,PE;1×10-6 mol/L)诱导的血管收缩功能的反应。结果:PO(4.05×10-9～4.05×10-5 mol/L)可浓度依赖性地抑制Ach诱导的EDR反应,对SNP诱导的非内皮依赖性舒张功能没有影响。GST(10,30或100μmol/L)可减轻PO(4.05×10-6 mol/L)对EDR的抑制作用,且GST浓度为10～30μmol/L时,该作用具有剂量效应;但GST对SNP诱导的非内皮依赖性舒张反应没有影响。各浓度GST与PO共同孵育血管环,可浓度依赖性地抑制PE诱导的血管收缩。结论:GST可抑制PO诱导的EDR受损,并抑制PE诱导的血管收缩效应。
Objective: To investigate the protective effects of genistein (GST) on the vascular dysfunction induced by paraoxon (PO). Methods: Isolated aortic rings were prepared from the thoracic aorta of male Sprague-Dawley rats and the tension of the vascular rings was measured and recorded. The experimental groups were as follows: 1) Vehicle control group, 0.1% dimethyl sulfoxide (DMSO) was used to pre-incubate the vascular rings for 30 min to detect the effect of rat thoracic aortic rings on acetylcholine (Ach; 1 × 10 -9 ~ 1 × 10-5 mol / L) induced endothelium-dependent relaxation (EDR) function and non-endothelial cells induced by sodiumnitroprusside (SN P; 1 × 10-6 mol / L) Dependent vasodilation; 2) After pre-incubation of vascular rings with various concentrations of PO (4.05 × 10-9 ~ 4.05 × 10-5 mol / L) for 30 min, 3) PO + GST treatment group, respectively, with PO (4.05 × 10-6 mol / L) and different concentrations of GST (1,3,10,30 or 100 μmol / L) for 30 min. The responses of rat thoracic aorta rings to Ach and SN P-induced vasodilatation and the effects of phenylephrine (PE; 1 × 10-6 mol / L) Induced vasoconstrictive response. Results: PO (4.05 × 10-9 ~ 4.05 × 10-5 mol / L) could inhibit Ach-induced EDR in a concentration-dependent manner and had no effect on SNP-induced non-endothelium-dependent diastolic function. GST (10, 30 or 100 μmol / L) could reduce the inhibitory effect of PO (4.05 × 10-6 mol / L) on EDR. When GST concentration was 10 ~ 30μmol / L, Induction of non-endothelium-dependent relaxation did not affect. GST and PO co-incubated with each concentration of vascular rings, concentration-dependent inhibition of PE-induced vasoconstriction. Conclusion: GST can inhibit PO-induced EDR damage and inhibit PE-induced vasoconstriction.