首页> 外文期刊>Journal of Traditional and Complementary Medicine >Mechanisms involved in the endothelium-dependent vasodilatory effect of an ethyl acetate fraction of Cyathea phalerata Mart. in isolated rats’ aorta rings
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Mechanisms involved in the endothelium-dependent vasodilatory effect of an ethyl acetate fraction of Cyathea phalerata Mart. in isolated rats’ aorta rings

机译:依赖于内皮依赖性血管舒张的机制 mart。在孤立的大鼠的主动脉戒指

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The speciesCyathea phalerataMart. is a tree fern, commonly known as “xaxim”, which is found in tropical and subtropical areas of Brazil. The present study investigated the mechanisms related with the vasorelaxant effects of an Ethyl Acetate Fraction (EAF) obtained fromC.?phaleratain rats’ thoracic aorta rings. In pre-contracted vessels, EAF (0.1–1000?μg/mL) caused a concentration-dependent relaxation. The endothelium denudation, the nitric oxide (NO) synthase and guanylyl cyclase inhibitor reduced the vasodilation, indicating the participation of NO/cGMP pathway in its effect. The relaxation of EAF was abolished in the absence of extracellular Ca2+and was significantly decreased in the presence of Ca2+entry blocker, suggesting that Ca2+influx plays an important role in EAF effect and probably in eNOS activity. However, the PI3K/Akt pathway is not responsible for eNOS phosphorylation/activation. The vasodilator effect of EAF was partially inhibited by KCl 40?mM and almost totally abolished with L-NOARG?+?KCl 40?mM, indicating also the role of hyperpolarization in its effect. Calcium activated K+channels are not involved in the EAF-induced hyperpolarization. The COX inhibitor, indomethacin, slightly reduced the vasodilation induced by EAF. In addition, EAF did not alter the relaxant effects of NO-donor, indicating that the relaxant activity cannot be attributed to free radical-scavenging properties. In conclusion, the present study showed that the EAF, causes an endothelium-dependent vasorelaxant effect in aorta that mainly involves the NO-cGMP pathway, hyperpolarization and prostanoids. The vasorelaxant activity of EAF can be attributed to the occurrence of polyphenol compounds.
机译:Speciescyathea Phaleratamart。是一棵树蕨,通常被称为“Xaxim”,它位于巴西的热带和亚热带地区。本研究研究了与乙酸乙酯级分(EAF)的血管内施差有关的机制,得到了从C的胸腺系胸部主动脉圈。在预收缩的血管中,EAF(0.1-1000Ω·μg/ ml)引起浓度依赖性的弛豫。内皮剥落,一氧化氮(NO)合成酶和陀螺环化酶抑制剂降低了血管舒张,表明NO / CGMP途径的参与其作用。在没有细胞外Ca2 +的情况下废除EAF的松弛,并且在CA2 +入口阻断程序存在下显着降低,表明CA2 +流入在EAF效应中发挥着重要作用,并且可能在eNOS活动中起着重要作用。然而,PI3K / AKT途径不对ENOS磷酸化/激活负责。 EAF的血管扩张作用由KCl 40×40μm抑制,几乎完全废除L-Noarg?+ +αmm,表明Hyperpolaratization在其作用中的作用。钙活化的K +通道不参与EAF诱导的超极化。 Cox抑制剂,吲哚美辛,略微减少了EAF诱导的血管舒张。此外,EAF没有改变禁止供体的弛豫效果,表明松弛活性不能归因于自由基清除性质。总之,本研究表明,EAF导致主动脉中的内皮依赖性血管链轴效应,主要涉及NO-CGMP途径,超极化和前列醇。 EAF的迁移活性可归因于多酚化合物的发生。

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