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丹参酮 IIA 改善慢性间歇性低氧大鼠的血管内皮功能障碍。

Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia.

机构信息

Department of Pharmacology, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, People's Republic of China.

Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, People's Republic of China.

出版信息

Cardiovasc Pathol. 2017 Nov-Dec;31:47-53. doi: 10.1016/j.carpath.2017.06.008. Epub 2017 Jun 30.

Abstract

Chronic intermittent hypoxia (CIH) during repetitive airflow cessations may cause endothelial dysfunction. Tanshinone IIA (Tan IIA) has been used to treat various circulatory disturbance-related diseases because of its pharmacological actions, including vasodilation. However, the mechanism of the effect of its vasodilation is not well established. The objective of this study was to explore the effect of Tan IIA in endothelium-dependent contracting factors and endothelin receptors in aortic endothelial dysfunction in CIH rats. Aortas of rats were retrieved for use in in vitro experiments (isometric force measurement), histological analysis, immunohistochemistry, and Western blotting. Tan IIA treatment increased the expression of endothelial nitric oxide synthase (eNOS) and formation of nitric oxide (NO), inhibited the production of endothelin-1 (ET-1), down-regulated ET receptor expression, and up-regulated ET receptor expression. In conclusion, Tan IIA protects endothelial function by inhibiting strain-induced ET-1 expression, decreasing ET receptors, increasing ET receptors, increasing the formation of NO, and up-regulating eNOS in CIH.

摘要

慢性间歇性低氧(CIH)在反复气流停止期间可能导致内皮功能障碍。丹参酮 IIA(Tan IIA)因其药理学作用,包括血管舒张作用,已被用于治疗各种与循环障碍相关的疾病。然而,其血管舒张作用的机制尚未得到很好的建立。本研究旨在探讨 Tan IIA 在 CIH 大鼠主动脉内皮功能障碍中内皮依赖性收缩因子和内皮素受体的作用。从大鼠中取出主动脉用于体外实验(等长力测量)、组织学分析、免疫组织化学和 Western blot。Tan IIA 治疗增加了内皮型一氧化氮合酶(eNOS)的表达和一氧化氮(NO)的形成,抑制了内皮素-1(ET-1)的产生,下调了 ET 受体的表达,并上调了 ET 受体的表达。总之,Tan IIA 通过抑制应变诱导的 ET-1 表达、减少 ET 受体、增加 ET 受体、增加 NO 的形成以及上调 eNOS 来保护内皮功能。

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