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
1 Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Av. Agustín Melgar s/n, Col Buenavista, C.P. 24039, Campeche, México
2 Facultad de Nutrición, Universidad Veracruzana, Médicos y Odontologos s/n C.P. 91010, Unidad del Bosque, Xalapa, Veracruz, México
3 Instituto de Investigaciones Psicológicas, Universidad Veracruzana, Av. Dr. Luis Castelazo Ayala s/n Col Industrial Animas, C.P. 91190, Xalapa, Veracruz, México
4 Escuela Nacional de Ciencias Biológicas del Instituto, Politécnico Nacional. Prol. Carpio y Plan de Ayala s/n Col. Santo Tomas, D.F. C.P. 11340, México
Abstract
Objective:
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).
Methods:
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.
Results:
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.
Conclusion:
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.
Keywords: Amino-steroid-anthracenone, Ischemia, Reperfusion, cAMP, Adenosine, ZM-241385.
Article Information
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
© 2018 Lauro et al.
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.
* Address correspondence to these authors at the Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Av. Agustín Melgar s/n, Col Buenavista, C.P. 24039, Campeche, México; Facultad de Nutrición, Universidad Veracruzana, Médicos y Odontologos s/n C.P. 91010, Unidad del Bosque, Xalapa, Veracruz, México; Tel: 9818119800; E-mails: lauro_1999@yahoo.com, rosasnm@yahoo.com.mx
Open Peer Review Details |
Manuscript submitted on 25-5-2018 |
Original Manuscript |
New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model |