ArticleClinical and experimental immunology2023
Effect and mechanisms of dexmedetomidine combined with macrophage migration inhibitory factor inhibition on the expression of inflammatory factors and AMPK in mice.
Article in Clinical and experimental immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Imperatorin ameliorates myocardial ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress-mediated apoptosis via the PI3K/AKT/Nrf2 pathway.Journal of cell communication and signaling · 2026Article
- Methyl rosmarinate alleviates myocardial ischemia-reperfusion injury in mice via triggering TGR5/AMPK signaling axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Novel function of macrophage migration inhibitory factor in regulating post-infarct inflammation and the therapeutic significance.Journal of advanced research · 2026Article
- Retrospective analysis and prediction model for vascular and nerve injuries in elderly patients following total knee arthroplasty.American journal of translational research · 2026Article
- The distinct functions of MIF in inflammatory cardiomyopathy.Frontiers in immunology · 2025Review
- Differential effects of dexmedetomidine on Gram-positive and Gram-negative bacterial killing and phagocytosis.International immunopharmacology · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Reperfusion after acute myocardial infarction can cause ischemia/reperfusion (I/R) injury, which not only impedes restoration of the functions of tissues and organs but may also aggravate structural tissue and organ damage and dysfunction, worsening the patient's condition. Thus, the mechanisms that underpin myocardial I/R injury need to be better understood. We aimed to examine the effect of dexmedetomidine on macrophage migration inhibitory factor (MIF) in cardiomyocytes from mice with myocardial I/R injury and to explore the mechanistic role of adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling in this process. Myocardial I/R injury was induced in mice. The expression of serum inflammatory factors, reactive oxygen species (ROS), adenosine triphosphate (ATP), and AMPK pathway-related proteins, as well as myocardial tissue structure and cell apoptosis rate, were compared between mice with I/R injury only; mice with I/R injury treated with dexmedetomidine, ISO-1 (MIF inhibitor), or both; and sham-operated mice. Dexmedetomidine reduced serum interleukin (IL)-6 and tumor necrosis factor-α concentrations and increased IL-10 concentration in mice with I/R injury. Moreover, dexmedetomidine reduced myocardial tissue ROS content and apoptosis rate and increased ATP content and MIF expression. MIF inhibition using ISO-1 reversed the protective effect of dexmedetomidine on myocardial I/R injury and reduced AMPK phosphorylation. Dexmedetomidine reduces the inflammatory response in mice with I/R injury and improves adverse symptoms, and its mechanism of action may be related to the MIF-AMPK pathway.
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