ArticleDrug design, development and therapy2021
High-Dose Dexmedetomidine Promotes Apoptosis in Fetal Rat Hippocampal Neurons.
Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Cognitive and Pyroptotic Outcomes of Neonatal Ketamine and Dexmedetomidine: Potential Neuroprotection via Caspase-1 Modulation.Developmental neurobiology · 2026Article
- The anticancer properties of dexmedetomidine in papillary thyroid cancer and its underlying mechanisms.Scientific reports · 2026Article
- Effects of Dexmedetomidine Treatment After Cerebral Ischemia/Reperfusion on Apoptosis and Oxidative Stress: A Rat Model.Life (Basel, Switzerland) · 2026Article
- Research status and advances in dexmedetomidine for sepsis‑induced multiple organ dysfunction syndrome (Review).International journal of molecular medicine · 2025Review
- Dexmedetomidine activates mitophagy and protects against pyroptosis in oxygen-glucose deprivation/reperfusion-induced brain damage via PINK1/Parkin pathway activation.Journal of bioenergetics and biomembranes · 2025Article
- Propofol and Dexmedetomidine Ameliorate Endotoxemia-Associated Encephalopathy via Inhibiting Ferroptosis.Drug design, development and therapy · 2024Article
- Role of ferroptosis in hypoxic preconditioning to reduce propofol neurotoxicity.Frontiers in pharmacology · 2023Article
- Dexmedetomidine attenuates subarachnoid hemorrhage-induced acute lung injury through regulating autophagy and TLR/NFκB signaling pathway.Korean journal of anesthesiology · 2022Article
- The propofol-induced mitochondrial damage in fetal rat hippocampal neurons via the AMPK/P53 signaling pathway.Annals of translational medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDexmedetomidine (DEX) is a potent a2-adrenoceptor agonist that has sedative, analgesic, and anxiolytic effects. Its primary clinical use is as an adjunct to general anesthesia to reduce anesthetic doses, provide analgesia and sedation in the preoperative and postoperative periods, it also used in intensive care units (ICUs). However, high concentrations of DEX may have toxic effects on neurons and cause neuronal apoptosis. This study aimed to evaluate the potential proapoptotic effects of DEX on fetal rat hippocampal neurons.
methodsPrimary hippocampal were cultured in vitro for 8 days and incubated with different DEX concentrations for 3 h. Cell viability was measured using cell counting kit-8 assays. Cell apoptosis was evaluated using flow cytometry. The expression of apoptosis-related proteins, such as cleaved caspase-3, caspase-9, Cyt-c, Bax, and Bcl-2, was measured by Western blotting. The mitochondrial ATP levels, Δψm, and ROS analyzed were conducted.
resultsHigh concentrations of DEX (≥100 μM) significantly reduced cell viability, induced neuronal apoptosis, upregulated the protein expression of cleaved caspase 3, Bax, cleaved caspase 9, and Cyt-c. DEX also considerably promoted the release of ROS. However, DEX (≥100 μM) downregulated the protein expression of Bcl-2, decreased the mitochondrial membrane potential (MTP), and reduced ATP synthesis.
conclusionHigh concentrations of dexmedetomidine produced toxic effects on neurons and caused neuronal apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.