ArticleOxidative medicine and cellular longevity2022
Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons.
Article in Oxidative medicine and cellular longevity, 2022. 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, 17 citations in OpenAlex.
- Hypoxia Triggers BNIP3/BNIP3L-Associated Mitophagy in HT22 Immortalized Hippocampal Neurons: A Temporal Descriptive Study.Biology · 2026Article
- Propofol regulates SLC6A2 expression via NAT10-mediated ac4C modification to modulate excessive mitophagy and hippocampal neuron dysfunction in aged postoperative cognitive dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Regulation of mitochondrial dynamics and function by melatonin type 1 receptor in parkinson's disease.Cellular and molecular life sciences : CMLS · 2025Article
- Modulating mitochondrial metabolism: a neuroprotective mechanism for hypoxic-ischemic preconditioning.Cell regeneration (London, England) · 2025Review
- Bidirectional Relationship Between Anaesthetic Drugs and Metabolic Syndrome: Clinical Effects and Mechanisms.Journal of cellular and molecular medicine · 2025Review
- Synthetic and semi-synthetic antioxidants in medicine and food industry: a review.Frontiers in pharmacology · 2025Review
- Acute Lung Injury and the NLRP3 Inflammasome.Journal of inflammation research · 2024Review
- Dexmedetomidine Attenuates Apoptosis and Neurological Deficits by Modulating Neuronal NADPH Oxidase 2-Derived Oxidative Stress in Neonates Following Hypoxic Brain Injury.Antioxidants (Basel, Switzerland) · 2022Article
- The Mechanism of TNF-Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia may induce mitochondrial abnormality, which is associated with a variety of clinical phenotypes in the central nervous system. Propofol is an anesthetic agent with neuroprotective property. We examined whether and how propofol protected hypoxia-induced mitochondrial abnormality in neurons.
methodsPrimary rat hippocampal neurons were exposed to propofol followed by hypoxia treatment. Neuron viability, mitochondrial morphology, mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) production were measured. Mechanisms including reactive oxygen species (ROS), extracellular regulated protein kinase (ERK), protein kinase A (PKA), HIF-1
resultsHypoxia increased intracellular ROS production and induced mPTP opening, while reducing ATP production, MMP values, and neuron viability. Hypoxia impaired mitochondrial dynamic balance by increasing mitochondrial fragmentation. Further, hypoxia induced the translocation of HIF-1
conclusionsIn rat hippocampal neurons, hypoxia induced oxidative stress, caused mitochondrial dynamic imbalance and malfunction, and reduced neuron viability. Propofol protected mitochondrial abnormality and neuron viability via antioxidant property, and the molecular mechanisms involved HIF-1
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