ArticleHeliyon2023
Dexmedetomidine combined with propofol attenuates myocardial ischemia/reperfusion injury by activating the AMPK signaling pathway.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Yixinyuan Gaofang ameliorates myocardial infarction in rats by inhibiting the TNF/NF-κB pathway.Scientific reports · 2026Article
- The mechanism of dexmedetomidine regulation of the HIF-1α/FUNDC1 axis in myocardial ischemia/reperfusion injury.Histology and histopathology · 2025Article
- Contactin -Associated protein1 Regulates Autophagy by Modulating the PI3K/AKT/mTOR Signaling Pathway and ATG4B Levels in Vitro and in Vivo.Molecular neurobiology · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Myocardial ischemia/reperfusion (MI/R) injury is a major cause of cardiac tissue damage, with high disability and death rates. Although both dexmedetomidine (Dex) and propofol (PPF) have been indicated to alleviate MI/R injury in rat models, the effects of the combined use of these two drugs remain unclear. This study aimed to investigate the combined effects of Dex and PPF against MI/R injury and related mechanisms. Methods: A rat model of MI/R injury was established and used to explore the combined effects of Dex and PPF on MI/R injury. Hematoxylin-eosin (HE) and Masson staining were used for histopathological evaluation. 2,3,5-triphenyltetrazolium chloride (TTC), echocardiography, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining were used to determine myocardial infarction size, cardiac function, and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) was performed to assess myocardial function and oxidative stress (OS). Autophagy was observed through transmission electron microscopy. Moreover, western blotting was conducted to detect autophagy markers and the AMPK pathway. Results: The combination of Dex and PPF alleviated histopathological injury, reduced myocardial infarction, and rescued cardiac dysfunction in MI/R rats. Furthermore, Dex combined with PPF decreased the levels of MDA and ROS and increased the SOD level in MI/R rats. Besides, Dex combined with PPF inhibited myocardial apoptosis in MI/R rats. After combined treatment with Dex and PPF, the number of autophagosomes, expression levels of Beclin-1 and LC3II/LC3I were elevated, while the expression levels of p62 were reduced in MI/R rats. The combined use of Dex and PPF activated the AMPK pathway in MI/R rats. Compound C (an AMPK inhibitor) could abolish the combined effects of Dex and PPF on alleviating myocardial injury and enhancing autophagy in MI/R rats. Conclusion: The combination of Dex and PPF attenuated MI/R injury in rats, which may be associated with the activation of the AMPK signaling pathway.
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