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白蒿通过激活NO/cGMP途径和K(ATP)通道舒张大鼠主动脉。

Artemisia herba-alba Asso relaxes the rat aorta through activation of NO/cGMP pathway and K(ATP) channels.

作者信息

Skiker Mounia, Mekhfi Hassane, Aziz Mohamed, Haloui Benyounes, Lahlou Saad, Legssyer Abdelkhaleq, Bnouham Mohamed, Ziyyat Abderrahim

机构信息

Laboratoire de Physiologie et Ethnopharmacologie, Département de Biologie, Faculté des Sciences, Université Mohamed Premier.

出版信息

J Smooth Muscle Res. 2010;46(3):165-74. doi: 10.1540/jsmr.46.165.

Abstract

Artemisia herba-alba Asso (Compositae) is used in oriental Morocco to treat diabetes and arterial hypertension. The present work evaluated the vasorelaxant effect of Artemisia herba-alba aqueous extract (AHAE) in isolated rat aorta and the mechanism underlying this effect. In endothelium-containing aorta preparations, AHAE (10(-3), 10(-2), 10(-1), 1 and 2 mg/mL) relaxed the contraction elicited by noradrenaline in a concentration-dependent manner. This effect is dependent upon integrity of the vascular endothelium as it was fully abolished in endothelium-denuded preparations. The vasorelaxant effect of AHAE (2 mg/mL) was also inhibited by N(G)-nitro-L-arginine methyl-ester (100 microM), methylene blue (10 microM) or 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (50 microM) but not by 10 microM atropine. This effect remained unchanged by tetraethylammonium (5 mM) or indomethacin (10 microM) whereas it was significantly attenuated by glibenclamide (10 microM). These results suggest that AHAE produces an endothelium-dependent relaxation of the isolated rat aorta, an effect that seems mainly mediated through stimulation of the endothelial nitric oxide synthase by mechanisms other than activation of muscarinic receptors. Activation of ATP-dependent potassium channels partly contributes in the mediation of AHAE-induced endothelium-dependent relaxation.

摘要

摩洛哥东部地区使用白蒿(菊科)来治疗糖尿病和动脉高血压。本研究评估了白蒿水提取物(AHAE)对离体大鼠主动脉的血管舒张作用及其作用机制。在含有内皮的主动脉制剂中,AHAE(10⁻³、10⁻²、10⁻¹、1和2 mg/mL)以浓度依赖性方式舒张去甲肾上腺素引起的收缩。这种作用依赖于血管内皮的完整性,因为在内皮剥脱的制剂中这种作用完全消失。AHAE(2 mg/mL)的血管舒张作用也受到N(G)-硝基-L-精氨酸甲酯(100 μM)、亚甲蓝(10 μM)或1H-[1,2,4]恶二唑并[4,3-a]喹喔啉-1-酮(50 μM)的抑制,但不受10 μM阿托品的抑制。四乙铵(5 mM)或吲哚美辛(10 μM)对这种作用没有影响,而格列本脲(10 μM)则使其显著减弱。这些结果表明,AHAE可使离体大鼠主动脉产生内皮依赖性舒张,这种作用似乎主要是通过刺激内皮型一氧化氮合酶,而非通过激活毒蕈碱受体的机制介导的。ATP依赖性钾通道的激活部分参与了AHAE诱导的内皮依赖性舒张的介导过程。

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