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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
