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作 者:孙涛[1] 杨鹏[1] 杨蒙蒙[1] 唐亚娟[1] 张琰[1]
机构地区:[1]第四军医大学唐都医院药学部,西安710038
出 处:《中国药师》2017年第10期1710-1712,1717,共4页China Pharmacist
基 金:国家自然科学基金项目(编号:81403170)
摘 要:目的:研究红车轴草总异黄酮对离体大鼠肠系膜动脉环的舒张作用。方法:将大鼠肠系膜动脉环挂在两个L型金属针间,在浴槽中加入血管收缩剂获得稳定收缩后,加入不同浓度的红车轴草总异黄酮和(或)阻断剂,采用离体血管张力描记技术记录大鼠肠系膜动脉的张力的变化。结果:红车轴草总异黄酮(0.001~1 mg·ml^(-1))可浓度依赖性舒张K+krebs液(60 mmol·L^(-1)K+)预收缩的正常大鼠肠系膜动脉,与溶剂对照(DMSO)相比差异有统计学意义(P<0.01);去除大鼠肠系膜动脉内皮可以显著抑制红车轴草总异黄酮诱导的血管舒张反应,与完整内皮组相比差异有统计学意义(P<0.01);使用Nω-硝基-L-精氨酸甲酯(LNAME,10^(-4)mol·L^(-1))孵育可以减弱红车轴草总异黄酮诱导的血管舒张反应,与溶剂对照(DMSO)相比差异有统计学意义(P<0.01);而吲哚美辛(10^(-5)mol·L^(-1))对红车轴草总异黄酮诱导的血管舒张反应的影响无显著差异(P>0.05)。结论:红车轴草总异黄酮可以舒张离体肠系膜动脉,其机制可能与促进血管内皮释放一氧化氮有关。Objective:To investigate the vasorelaxant effect of the isoflavones in red clover on rat mesenteric artery rings. Meth-ods:The rat mesenteric artery rings were placed between two L form metal needles. When stable precontractions induced by vasocon-strictor were got, the different concentrations of isoflavones in red clover and ( or) blocker were added to the baths. The isometric ten-sion of the rat mesenteric artery rings was recorded using a myograph system. Results:The isoflavones in red clover could concentra-tion-dependently relax the rat mesenteric artery rings pre-contracted by K+krebs solution (60 mmol·L-1K+), and compared with the control group (Dmso), the difference was statistically significant (P〈0. 01). The isoflavones in red clover-induced relaxation was re-duced by the removal of endothelium, and compared with the complete endothelial group, the difference was statistically significant ( P〈0. 01). Pretreatment with Nω-nitro-L-arginine-methylesterhydrochloride (L-NAME,10 -4 mol·L-1) could suppress the relaxing re-sponse to the isoflavones in red clover, and compared with the control group, the difference was statistically significant (P〈0. 01). However, indomethacin(10 -5 mol·L-1) did not significantly affect the relaxation induced by the isoflavones in red clover (P 〉0. 05). Conclusion:The vasorelaxant effect of the isoflavones in red clover is through promoting nitric oxide release from vascular en-dothelium.
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