Abstract
BackgroundIntestinal ischemia/reperfusion (I/R) injury commonly occurs during perioperative periods, resulting in high morbidity and mortality on a global scale. Dexmedetomidine (Dex) is a selective α2-agonist that is frequently applied during perioperative periods for its analgesia effect; however, its ability to provide protection against intestinal I/R injury and underlying molecular mechanisms remain unclear.MethodsTo fill this gap, the protection of Dex against I/R injury was examined in a rat model of intestinal I/R injury and in an inflammation cell model, which was induced by tumor necrosis factor-alpha (TNF-α) plus interferon-gamma (IFN-γ) stimulation.ResultsOur data demonstrated that Dex had protective effects against intestinal I/R injury in rats. Dex was also found to promote mitophagy and inhibit apoptosis of enteric glial cells (EGCs) in the inflammation cell model. PINK1 downregulated p53 expression by promoting the phosphorylation of HDAC3. Further studies revealed that Dex provided protection against experimentally induced intestinal I/R injury in rats, while enhancing mitophagy, and suppressing apoptosis of EGCs through SIRT3-mediated PINK1/HDAC3/p53 pathway in the inflammation cell model.ConclusionHence, these findings provide evidence supporting the protective effect of Dex against intestinal I/R injury and its underlying mechanism involving the SIRT3/PINK1/HDAC3/p53 axis.
Highlights
Intestinal ischemia/reperfusion (I/R) injury commonly occurs during perioperative periods, resulting in high morbidity and mortality on a global scale
Ischemia–reperfusion (I/R) injury reportedly occurs as a result of interruption of organ blood flow and subsequent restoration; this pathophysiology accounts for other pathologies including stroke, myocardial infarction, renal I/R injury, intestinal I/R injury and liver I/R injury, making it a cause of disability or mortality in severe cases [1]
Dex treatment reduces oxidative stress and protects rats against experimentally induced intestinal I/R injury First, we established a rat model of intestinal I/R injury by inducing superior mesenteric artery (SMA) occlusion followed by injection with
Summary
Intestinal ischemia/reperfusion (I/R) injury commonly occurs during perioperative periods, resulting in high morbidity and mortality on a global scale. Dexmedetomidine (Dex) is a selective α2-agonist that is frequently applied during perioperative periods for its analgesia effect; its ability to provide protection against intestinal I/R injury and underlying molecular mechanisms remain unclear. Ischemia–reperfusion (I/R) injury reportedly occurs as a result of interruption of organ blood flow and subsequent restoration; this pathophysiology accounts for other pathologies including stroke, myocardial infarction, renal I/R injury, intestinal I/R injury and liver I/R injury, making it a cause of disability or mortality in severe cases [1]. The limitations that exist regarding the pathophysiology of intestinal I/R injury has made the development of effective methods for prevention and treatment extremely challenging [5]. The role of dexmedetomidine (Dex) in the treatment of intestinal I/R injury has been highlighted in recent studies, which could be a potential agent for intestinal I/R injury prevention [6]
Sign-in/Register to view highlights & summary 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.
