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Arctigenin improves vascular tone and decreases inflammation in human saphenous vein

机译:甲基氨基素改善血管间调并降低人静脉静脉的炎症

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Abstract The goal of this study was to test the effects of bioactive phenylpropanoid dibenzylbutyrolactone lignan arctigenin (ATG) in vascular tone. Human bypass graft vessel, from a saphenous vein (SV), were set up in organ bath system and contracted with potassium chloride (KCl, 40 mM). Two concentration–response curves of noradrenaline (NE) (10 nM–100 μM) separated with an incubation period of 30 min without (Control) or with ATG (3–100 μM) were established. Inhibitors of nitric oxide, prostaglandins, K + related channels or calcium influx were used to delineate the molecular mechanisms beyond ATG effects. To investigate anti-inflammatory actions, SV were treated with 10 μM or 100 μM ATG and incubated for 18 h in the absence or presence of both interleukin-1beta (IL-1β) and lipopolysaccharide (LPS) to mimic the physiological or inflamed tissue conditions. Proatherogenic and inflammatory mediators ?nterleukine-1 beta (IL-1β), Monocyte Chemoattractant Proteine-1 (MCP-1), Tumor Necrosis Factor- α (TNF-α), ?nterleukine-6 (IL-6), Prostaglandin E 2 (PGE 2 ) and ?nterleukine-8 (IL-8) in the supernatant were measured. ATG significantly decreased vascular contractile response to NE. Moreover, it reduced contractions induced by KCl and cumulative addition of CaCl 2. The mediators were significantly increased in inflammatory conditions compared to normal conditions, an effect which was inhibited by ATG (10 and 100 μM). ATG reduces contractions in SV and decreases the production of proinflammatory-proatherogenic mediators, setting the stage for further evaluating the effect of ATG in cardiovascular diseases. ]]>
机译:摘要本研究的目标是测试生物活性苯丙烷二苄基丁胺酮(ATG)以血管间调的影响。从隐式静脉(SV)中,人旁路移植件在器官浴系统中设置并用氯化钾(KCl,40mm)收缩。建立了在没有(对照)或用ATG(3-100μm)的30分钟的孵育期分离的去甲肾上腺素(NE)(NO)(10nm-100μm)的两个浓度 - 反应曲线。一氧化氮,前列腺素,K +相关通道或钙流入的抑制剂用于描绘ATG效应之外的分子机制。为了研究抗炎作用,将SV用10μm或100μmAtg处理,在白细胞介素-1beta(IL-1β)和脂多糖(LPS)的情况下孵育18小时,以模拟生理或发炎的组织条件。 proatherogenc和炎症介质?Nterleukine-1β(IL-1β),单核细胞化学蛋白蛋白-1(MCP-1),肿瘤坏死因子 - α(TNF-α),?奈瑟酮-6(IL-6),前列腺素E 2测量上清液中的(PGE 2)和αNterleukine-8(IL-8)。 ATG对NE的血管收缩响应显着降低。此外,它降低了KCl诱导的收缩和CaCl 2的累积添加。与正常条件相比,肿瘤在炎性条件下显着增加,该效果被ATG(10和100μm)抑制。 ATG减少了SV中的收缩,降低了促炎前植物介质的产生,用于进一步评估ATG在心血管疾病中的效果的阶段。 ]]>

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