New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model
Figueroa-Valverde Lauro1, *, Rosas-Nexticapa Marcela2, *, Mateu-Armand Virginia2, Herrera-Meza Socorro3, Díaz-Cedillo Francisco4, Montano-Tapia Elizabeth2, García-Cervera Elodia1, Pool-Gómez Eduardo1, Hau-Heredia Lenin1, García-Martínez Rolando1, Lopez-Ramos Maria1, Cauich-Carrillo Regina1, Parra-Galindo Perla2
Identifiers and Pagination:Year: 2018
First Page: 10
Last Page: 20
Publisher Id: TOPHARMJ-8-10
Article History:Received Date: 25/5/2018
Revision Received Date: 8/9/2018
Acceptance Date: 15/9/2018
Electronic publication date: 17/10/2018
Collection year: 2018
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.