| 王为民,虞燕琴,钱令波,舒强,刘广义,林茹,杨军.大黄素对大鼠体外血管内皮一氧化氮cGMP信号途径的影响[J].,2006,(7):636-639 |
| 大黄素对大鼠体外血管内皮一氧化氮cGMP信号途径的影响 |
| Effect of Emodin on NO-cGMP Signal Pathway in Rat Vascular Endothelium in vitro |
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| DOI： |
| 中文关键词: 大黄素 主动脉 血管内皮 一氧化氮 |
| 英文关键词:emodin aortic rings vascular endothelium nitric oxide |
| 基金项目:国家自然科学基金(No.30500413);中国博士后科学基金(No.2004036149) |
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| 中文摘要: |
| 目的探讨大黄素的舒血管效应与血管内皮一氧化氮cGMP信号途径的关系。方法采用MedLab生物信号采集系统记录灌流大鼠胸主动脉环张力变化;用硝酸还原酶法测定大黄素处理后离体大鼠主动脉血管的总一氧化氮合酶(tNOS)、结构型一氧化氮合酶(cNOS)、诱导型一氧化氮合酶(iNOS)活性的变化。结果大黄素对苯肾上腺素和氯化钾预收缩的内皮完整和去内皮血管环具有浓度依赖性的舒张作用。非特异性钾通道抑制剂氯化铯预处理能显著减弱大黄素对去内皮血管环的舒血管作用,但未能抑制大黄素对内皮完整血管环的舒血管作用。用一氧化氮合酶(NOS)抑制剂L-NAME和鸟苷酸环化酶抑制剂ODQ预处理后,40μmol/L大黄素引起的血管舒张作用被部分阻断,其血管舒张幅度分别为对照的(64·76±13·73)%和(6·28±4·79)%。40μmol/L大黄素处理能够使血管iNOS的活性显著升高。结论大黄素的内皮依赖性舒血管作用可能通过激活血管内皮细胞中一氧化氮/cGMP信号途径而实现。 |
| 英文摘要: |
| ObjectiveTo investigate the vaso relaxation effect of emodin and its relationship with NO-cGMP signal pathway . MethodsChanges of tension of rat thora cic aortic rings were measure d by MedLab biologic signal collection system, and the activity of total nitric oxide synthase (tNOS), constitutive NOS (cNOS) and inducible NOS (iNOS) in endot helium after being treated with emodin was determined with nitric acid re ductase method. ResultsEmodin relaxed the phenylephrine and potasium chlorate induced contraction of aortic rings, either with or without intact endothelium , in a concentration-dependent manner. Pretreatment of no-specific potassium channel blocker strontium chloride (CsCL) could attenuate the vasorelaxation effect of emodin on aortic rings without intact endothelium, but it could not i nhibit vasorelaxation of emodin on aortic rings with intact endothelium. This vasorelaxation action of emodin (40 μmol/L) could be partial blocked by NOS inhibitor L-NAME and guanylate cyclase inhibitor ODQ, with t he vasorelaxation range dropped to 64.76±13.73% and 6.28±4.79% respe ctive ly. Moreover, emodin (40 μmol/L) increased iNOS activity significantly. ConclusionThe concentration-dependent vasorelaxation e ffect of emodin might act by activating the NO-cGMP pathway in vascular endothelium. |
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