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Dexmedetomidine reduces myocardial ischemia-reperfusion injury in young mice through MIF/AMPK/GLUT4 axis
Siyu Chen1, Aimei Li1, Jianjiang Wu1
1Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, No.137, Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, Uygur Autonomous Region, China.
Background:
Reperfusion of ischemic tissue has adverse impact on the myocardium. Dexmedetomidine (Dex) is a α2-adrenergic receptor (α2-AR) agonist with sedative and analgesic effects. Macrophage migration inhibition factor (MIF) is a pressure-regulating cytokine and is responsible for inflammatory and immune diseases. This study aims to reveal the consequences of Dex on myocardial ischemia-reperfusion injury (IRI) in young mice.
Methods:
Fifty mice were raised and examined. At the end of the experiment, all mice were euthanized. The anterior descending department of the left coronary artery in mice was under ischemia for 60 min, then the ligation line was released and reperfused for 120 min to establish the IRI model. Mice were randomly divided into Sham, control, treatment using 4,5-dihydro-3-(4-hydroxyphenyl)-5-isoxazoleacetic acid (ISO-1), Dex treatment, and Dex combined ISO-1 treatment groups. Interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) and ATP levels were recorded. The expressions of MIF, P-adenosine monophosphate-activated kinase α (AMPKα), glucose transporter (GLUT)4, Bax and Bcl-2 were detected by Western Blot (WB). Hematoxylin and Eosin (H&E) staining was used to study cell morphology. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay. Echocardiography was carried out at the end of reperfusion, and the infarct size was calculated by Electron microscopy.
Results:
I/R + Dex group showed significantly increased IL-6 and TNF-α levels and reduced myocardial cell necrosis and apoptosis. H&E staining showed alleviated myocardial disorder, myocardial cell swelling, myocardial fiber fracture, and inflammatory cell infiltration in I/R + Dex group. Myocardial cell necrosis and apoptosis were significantly reduced in I/R + Dex group. ATP level in myocardial tissue of mice in I/R group was substantially decreased, while that in Dex group was increased. WB results showed that MIF, P-AMPK α, GLUT4 and Bcl-2 levels were increased and Bax levels were decreased in I/R + Dex group.
Conclusion:
Dex may exert myocardial protection in young mice through MIF/AMPK/GLUT4 axis.
Insights
Dexmedetomidine (Dex) protects young mice from heart damage after reperfusion injury. It reduces cell death and inflammation by influencing the MIF/AMPK/GLUT4 pathway.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Reperfusion of ischemic tissue can harm the myocardium.
- Dexmedetomidine (Dex) is an α2-AR agonist with sedative and analgesic properties.
- Macrophage migration inhibition factor (MIF) is a cytokine involved in inflammatory and immune responses.
Purpose of the Study:
- To investigate the protective effects of Dexmedetomidine (Dex) on myocardial ischemia-reperfusion injury (IRI) in young mice.
- To explore the underlying molecular mechanisms, including the role of MIF, AMPK, and GLUT4.
Main Methods:
- Established a myocardial IRI model in young mice.
- Administered Dexmedetomidine (Dex) and ISO-1 (MIF inhibitor) to different treatment groups.
- Assessed cardiac function, infarct size, inflammatory markers (IL-6, TNF-α), oxidative stress (ROS), ATP levels, cell apoptosis, and protein expression (MIF, AMPKα, GLUT4, Bax, Bcl-2) via ELISA, Western Blot, H&E staining, TUNEL assay, and echocardiography.
Main Results:
- Dexmedetomidine treatment significantly reduced myocardial cell necrosis and apoptosis.
- Dexmedetomidine increased IL-6 and TNF-α levels but alleviated myocardial disorder and inflammatory infiltration.
- Dexmedetomidine upregulated MIF, p-AMPKα, GLUT4, and Bcl-2, while downregulating Bax expression, and increased ATP levels.
Conclusions:
- Dexmedetomidine demonstrates myocardial protective effects in young mice subjected to IRI.
- The protective mechanism appears to involve the MIF/AMPK/GLUT4 signaling axis.
