ArticleCNS neuroscience & therapeutics2024
Drug-drug interactions between propofol and ART drugs: Inhibiting neuronal activity by affecting glucose metabolism.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude.Journal of neuroscience research · 2026Article
- Cardiovascular system characteristics in HIV/AIDS patients with talaromycosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Elevated Release of Presynaptic Glutamate: The Potential Pathogenesis of Anti-NMDAR Encephalitis-Associated Seizures.CNS neuroscience & therapeutics · 2025Article
- Rab11a-dependent recycling of Glut3 inhibits seizure-induced neuronal disulfidptosis by alleviating glucose deficiency.Cell & bioscience · 2025Article
- Molecular Precision Medicine: Application of Physiologically Based Pharmacokinetic Modeling to Predict Drug-Drug Interactions Between Lidocaine and Rocuronium/Propofol/Paracetamol.International journal of molecular sciences · 2025Article
- Exploring the Interaction of 3-Hydroxy-4-pyridinone Chelators with Liposome Membrane Models: Insights from DSC and EPR Analysis.Molecules (Basel, Switzerland) · 2024Article
- Drug-drug interactions between propofol and ART drugs: Inhibiting neuronal activity by affecting glucose metabolism.CNS neuroscience & therapeutics · 2024Article
- Association between lactate metabolism‑related molecules and venous thromboembolism: A study based on bioinformatics and anExperimental and therapeutic medicine · 2024Article
- NDUFA11 may be the disulfidptosis-related biomarker of ischemic stroke based on integrated bioinformatics, clinical samples, and experimental analyses.Frontiers in neuroscience · 2024Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe use of two or more drugs carries the potential risk of drug-drug interactions (DDIs), which may result in adverse reactions. Some human immunodeficiency virus (HIV)-infected patients who receive antiretroviral therapy (ART) may require general anesthesia with propofol (PRL) before undergoing surgical treatment. Both PRL and ART drugs may lead to neuronal dysfunction, which can be accompanied by energy metabolism disorders. Neurons take in glucose mainly through glucose transporter 3 (Glut3) which is specifically expressed on the cell membranes of neurons. However, to date, no study has examined whether the DDIs of PRL and ART drugs interfere with glucose metabolism and Glut3 expression in neurons.
methodsAn in vitro model was constructed using the primary cultures of neurons. PRL and ART drugs (EFV, AZT, and 3TC), were added at different concentrations (low, medium, and high). The neurons were exposed to the drugs for 1, 4, 8, and 12 h. The optimal drug concentration and exposure time were selected. The cellular survival rate, glucose concentration, electrophysiology, and the expression of Glut3 were detected.
resultsThere were no significant changes in the cellular survival rates of the neurons that were exposed to both PRL and ART drugs at low concentrations for 1 h. However, the survival rates of the neurons decreased significantly as the drug concentrations and durations increased. The glucose concentration of the neurons that were exposed to both PRL and the ART drugs was significantly decreased. The glucose concentration of the neurons was not affected by any individual drug. The amplitude of the action potential and the expression of Glut3 were decreased in the neurons that were exposed to both PRL and ART drugs.
conclusionsThe main adverse reactions induced by the DDIs between PRL and the ART drugs were decreased glucose metabolism and neuronal damage, which were caused by inhibiting the expression of Glut3. More importantly, we found that decreases in glucose metabolism predated neuronal damage.
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