Why the study?
Does an Amino-Steroid-Anthracenone derivative reduce infarct area in a Wistar rat model of ischemia-reperfusion injury?
Does an Amino-Steroid-Anthracenone derivative reduce infarct area in a Wistar rat model of ischemia-reperfusion injury?
An amino-steroid-anthracenone derivative reduces ischemia-reperfusion injury in a rat model via A2 adenosine receptor activation.
ASA may limit infarct size in rat ischemia-reperfusion; hypothesis-generating for human cardioprotection.
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 A 2 adenosine receptor activation and these phenomena involve changes in cAMP levels.
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Lauro et al. (2018) studied this question.
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