Article Sidebar
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Dexmedetomidine preconditioning alleviates apoptosis in rat cardiomyocytes by suppressing programmed cell death 4 (PDCD4) after myocardial ischemia-reperfusion injury
Abstract
Purpose: To determine the role of dexmedetomidine (Dex) in hypoxia/reoxygenation (H/R)-induced myocardial cell injury and the possible involvement of the programmed cell death 4 (Pdcd4) gene in Dex-mediated myocardial cell apoptosis after ischemia-reperfusion (I/R) injury.
Methods: An in vivo I/R-injured rat model and in vitro H/R rat cell model were evaluated to ascertain the role of Dex in apoptosis. Programmed cell death 4 (PDCD4) gene expression levels were measured after Dex preconditioning. The effects of Pdcd4 knockdown or overexpression on Dex-mediated apoptosis during H/R injury were determined.
Results: Dex pretreatment alleviated myocardial infarction in rats, suppressed myocardial cell apoptosis, and inhibited PDCD4 expression (p < 0.05). Treatment with Dex also alleviated H/R-induced apoptosis in rat cardiomyocytes, while PDCD4 expression decreased after Dex treatment (p < 0.05). Moreover, PDCD4 overexpression reversed the inhibitory effect of Dex on H/R myocardial cell apoptosis.
Conclusion: Dex alleviates myocardial infarction in rats via its effect on PDCD4 expression. Therefore, Dex can potentially be used for the treatment but this has to clinical studies.
