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杰克根提取物致使大鼠主动脉环舒张的首次报告。

First Report of Jack Root Extract Causing Relaxation of Aortic Rings in Rats.

作者信息

Tee Bae Huey, Hoe See Ziau, Cheah Swee Hung, Lam Sau Kuen

机构信息

Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.

出版信息

Biomed Res Int. 2016;2016:1361508. doi: 10.1155/2016/1361508. Epub 2016 Oct 9.

DOI:10.1155/2016/1361508
PMID:27800486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5075299/
Abstract

Although has been studied for erectile function, the blood pressure- (BP-) lowering effect has yet to be verified. Hence, this study aims at investigating the BP-lowering properties of the plant with a view to develop an antihypertensive agent that could also preserve erectile function. Ethanolic root extract was partitioned by hexane, dichloromethane (DCM), ethyl acetate, butanol, and water. The DCM fraction, found to be potent in relaxing phenylephrine- (PE-) precontracted rat aortic rings, was further purified by column chromatography. Subfraction DCM-II, being the most active in relaxing aortae, was studied for effects on the renin-angiotensin and kallikrein-kinin systems in aortic rings. The effect of DCM-II on angiotensin-converting enzyme (ACE) activity was also evaluated . Results showed that DCM-II reduced ( < 0.05) the contractions evoked by angiotensin I and angiotensin II (Ang II). In PE-precontracted rings treated with DCM-II, the Ang II-induced contraction was attenuated ( < 0.05) while bradykinin- (BK-) induced relaxation enhanced ( < 0.001). , DCM-II inhibited ( < 0.001) the activity of ACE. These data demonstrate that the vasodilatory effect of DCM-II appears to be mediated inhibition of Ang II type 1 receptor and ACE as well as enhancement of Ang II type 2 receptor activation and BK activity.

摘要

尽管已对其勃起功能进行了研究,但其降压效果尚未得到证实。因此,本研究旨在研究该植物的降压特性,以期开发一种既能维持勃起功能又能降低血压的药物。乙醇根提取物用己烷、二氯甲烷(DCM)、乙酸乙酯、丁醇和水进行分配。发现DCM部分对去氧肾上腺素(PE)预收缩的大鼠主动脉环具有显著的舒张作用,通过柱色谱进一步纯化。在舒张主动脉方面活性最高的亚组分DCM-II,被用于研究其对主动脉环中肾素-血管紧张素和激肽释放酶-激肽系统的影响。还评估了DCM-II对血管紧张素转换酶(ACE)活性的影响。结果表明,DCM-II降低了(<0.05)血管紧张素I和血管紧张素II(Ang II)引起的收缩。在用DCM-II处理的PE预收缩环中,Ang II诱导的收缩减弱(<0.05),而缓激肽(BK)诱导的舒张增强(<0.001)。此外,DCM-II抑制了(<0.001)ACE的活性。这些数据表明,DCM-II的血管舒张作用似乎是通过抑制1型Ang II受体和ACE以及增强2型Ang II受体激活和BK活性介导的。

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Angiotensin-(1-9) reverses experimental hypertension and cardiovascular damage by inhibition of the angiotensin converting enzyme/Ang II axis.血管紧张素-(1-9)通过抑制血管紧张素转换酶/血管紧张素II轴来逆转实验性高血压和心血管损伤。
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