New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model

The Open Pharmacology Journal Pub Date : 2018-10-17 DOI:10.2174/1874143601808010010

Figueroa‐Valverde Lauro, Rosas-Nexticapa Marcela, Mateu-Armand Virginia, Herrera-Meza Socorro, D. Francisco, Montano-Tapia Elizabeth, García-Cervera Elodia, Pool-Gómez Eduardo, Hau-Heredia Lenin, García-Martínez Rolando, López-Ramos Maria, Cauich-Carrillo Regina, P. Perla

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引用次数: 1

Abstract

The main objective of this study was to evaluate the biological activity of an ASA (Amino-Steroid-Anthracenone derivative) against heart failure caused by the ischemia- reperfusion injury (translated as infarct area). Biological activity exerted by ASA (0.001-100 nM) on infarct area was determined using an ischemia-reperfusion injury model. In addition, to characterize the molecular mechanism involved in the effect exerted by ASA on left ventricular pressure, some drugs such as estrone (0.001-100 nM), tamoxifen (1 nM), butoxamine (1 nM) and ZM-241385 (1 nM) were used. The experimental data showed that ASA decreased the infarction area significantly (p = 0.05) compared to estrone. Other results indicated that ASA decreased left ventricular pressure and this effect was inhibited by ZM-241385. In addition, ASA increased cAMP levels in a time-dependent manner compared to control conditions. The results showed that ASA decreases ischemia-reperfusion injury (translated as infarct area) via A2 adenosine receptor activation and these phenomena involve changes in cAMP levels.

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具有抗Wistar大鼠缺血再灌注损伤生物活性的新型氨基甾体蒽酮

本研究的主要目的是评估ASA(氨基类固醇蒽酮衍生物)对缺血再灌注损伤(翻译为梗死区)引起的心力衰竭的生物活性。采用缺血再灌注损伤模型测定ASA (0.001 ~ 100 nM)对梗死面积的生物活性。此外，为了表征ASA对左室压影响的分子机制，我们使用了雌酮(0.001 ~ 100 nM)、他莫昔芬(1 nM)、丁胺(1 nM)和ZM-241385 (1 nM)等药物。实验数据显示，与雌酮相比，ASA可显著减少梗死面积(p = 0.05)。其他结果显示ASA降低左室压，ZM-241385可抑制这一作用。此外，与对照组相比，ASA以时间依赖性的方式增加cAMP水平。结果表明，ASA通过激活A2腺苷受体减少缺血再灌注损伤(即梗死面积)，这种现象与cAMP水平的变化有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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The Open Pharmacology Journal

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