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作 者:刘玉玲[1] 饶志威[1] 李震[1] 高治平[1] 黄红林[1]
机构地区:[1]南华大学药物药理研究所,湖南衡阳421001
出 处:《国际病理科学与临床杂志》2011年第6期471-475,共5页Journal of International Pathology and Clinical Medicine
基 金:湖南省高校创新平台开放基金(11K056)~~
摘 要: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 protective effect of genistein on damages of paraoxon-induced endothelium-dependent relaxation(EDR) in the rat thoracic aorta. Methods Thoracic aortas were isolated from 30 male SD rats.The isometric tension of the thoracic aorta rings was measured.The aortic rings were divided into the following groups: control group,the thoracic aorta rings was incubated with 0.1% dimethyl sulfoxide(DMSO) for 30 min.The acetylcholine(Ach;1×10-9-1×10-5 mol/L)-induced EDR and sodium nitroprusside(SNP;1×10-6 mol/L)-induced endothelium-independent relaxation were measured.Paraoxon groups,the rings were incubated with PO at the concentration of 4.05×10-9-4.05×10-5 mol/L for 30 min.The Ach-induced and SNP-induced relaxations were measured.PO+genistein groups,the rings were incubated with PO(4.05×10-6 mol/L) plus GST(1,3,10,30,or 100 μmol/L) for 30 min.The Ach-and SNP-induced relaxations and phenyllphrine(PE;1×10-6 mol/L)-induced contraction were measured. Results PO(4.05×10-9-4.05×10-5 mol/L) concentration-dependently inhibited Ach-induced EDR,but did not affect SNP-induced endothelium-independent relaxation of aortic isolated rings.GST at 10,30,or 100 μmol/L lessened the inhibition of Ach-induced EDR injured by PO(4.05×10-6 mol/L) and GST at 10-30 μmol/L had the concentration-dependent inhibitory effect.But GST did not affect SNP-induced endothelium-independent relaxation of aortic isolated rings.GST at 1-100 μmol/L also concentration-dependently inhibited PE-induced contraction of aortic isolated rings. Conclusion GST could inhibit PO-induced EDR injury and decrease PE-induced contraction.
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