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四羟基二苯乙烯葡萄糖苷通过内皮依赖性和非内皮依赖性机制引起肠系膜上动脉舒张。

Tetrahydroxystilbene glucoside-induced relaxation of the superior mesenteric artery via both endothelium-dependent and endothelium-independent mechanisms.

机构信息

Department of Chinese Materia Medica and Natural Medicines, Air Force Medical University, Xi'an 710032, Shanxi, China; Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an 710021, China.

Department of Chinese Materia Medica and Natural Medicines, Air Force Medical University, Xi'an 710032, Shanxi, China.

出版信息

Microvasc Res. 2019 May;123:42-49. doi: 10.1016/j.mvr.2018.10.007. Epub 2018 Oct 25.

DOI:10.1016/j.mvr.2018.10.007
PMID:30367840
Abstract

Tetrahydroxystilbene glucoside (TSG) is the main water-soluble component in Polygonum multiflorum Thunb, and it has many cardioprotective effects. Although TSG is able to relax blood vessels, its relaxation of rat superior mesenteric arteries and the underlying mechanism of this process are not clearly understood. The aim of the present study was to use in vivo and in vitro models to investigate the arterial relaxation effect of TSG on rat superior mesenteric arteries and the mechanisms involved. We found that TSG concentration-dependently relaxed the superior mesenteric artery with or without endothelium. The vasorelaxation induced by TSG is not related to the vasodilator derived factor NO but is rather by the inhibition of COX-2 activity and decreased TXA. We also found that the vasorelaxation induced by TSG was attenuated by 4‑AP. Moreover, TSG also inhibited the contraction induced by an increase in external calcium concentration in Ca-free medium plus KCl (60 mM). These results suggest that TSG induces relaxation in mesenteric arterial rings through an endothelium-dependent pathway that involves the inhibition of COX-2 activity and decreased in TXA and through an endothelium-independent pathway via opening of a voltage-dependent K channel, blockade of Ca influx and release of intracellular Ca.

摘要

二苯乙烯苷(TSG)是何首乌中主要的水溶性成分,具有多种心脏保护作用。虽然 TSG 能够舒张血管,但它对大鼠肠系膜动脉的舒张作用及其潜在机制尚不清楚。本研究旨在使用体内和体外模型来研究 TSG 对大鼠肠系膜动脉的动脉舒张作用及其涉及的机制。我们发现 TSG 浓度依赖性地舒张有或无内皮的肠系膜动脉。TSG 诱导的血管舒张与 NO 衍生的血管舒张因子无关,而是通过抑制 COX-2 活性和减少 TXA 来实现的。我们还发现,4-AP 可减弱 TSG 诱导的血管舒张。此外,TSG 还抑制了在无钙介质加 KCl(60mM)中由增加细胞外钙浓度引起的收缩。这些结果表明,TSG 通过涉及抑制 COX-2 活性和减少 TXA 的内皮依赖性途径以及通过开放电压依赖性 K 通道、阻断 Ca 内流和释放细胞内 Ca 的内皮非依赖性途径诱导肠系膜动脉环松弛。

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