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[目的]观察卫矛正丁醇提取物(BEA)对大鼠离体血管功能的影响,并探讨其机制.[方法]采用大鼠离体血管功能实验装置,分别记录血管张力变化.给予累加质量浓度(0.1~100.0mg/L)BEA,观察对去氧肾上腺素(PE,1.0μmol/L)预收缩有内皮和去内皮血管环的作用;采用不同阻断剂预处理后观察BEA对血管环张力改变的影响.[结果]BEA剂量依赖性地舒张PE预收缩的内皮完整的大鼠胸主动脉环.内皮去除、左旋硝基精氨酸甲酯和ODQ预处理可显著抑制BEA对内皮完整血管的舒张效应(P<0.05),而维拉帕米、地尔硫卓、吲哚美辛、格列本脲及TEA预处理未见明显抑制BEA诱导的血管舒张作用(P>0.05).[结论]BEA的内皮依赖性舒张血管作用主要是通过内皮依赖性NO-cGMP信号途径来实现.
[Objective] To observe the effect of butanol extract of Euonymus fortis (BEA) on the function of ex vivo vascular in rats and to explore its mechanism. [Methods] The rat vascular function experimental device was used to record the change of vascular tension. (0.1 ~ 100.0mg / L) BEA was used to observe the effect of BEA pretreatment on neovascularization of endothelium and endothelium-derived vascular rings. After pretreatment with different blockers, the effects of BEA on blood vessels [Results] The BEA dose-dependently relaxes the pre-contracted endothelium of rat thoracic aortic rings.Endothelial removals, L-NAME and ODQ preconditioning can significantly inhibit BEA to endothelial (P <0.05). No significant inhibition of BEA-induced vasodilatation was observed in verapamil, diltiazem, indomethacin, glibenclamide and TEA preconditioning (P> 0.05). [Conclusion] Endothelium-dependent vasodilatation of BEA occurs primarily through the endothelium-dependent NO-cGMP signaling pathway.