ArticleDrug design, development and therapy2018
Ketamine ameliorates oxidative stress-induced apoptosis in experimental traumatic brain injury via the Nrf2 pathway.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Protective effects of propofol, ketamine, and their combination against HScientific reports · 2026Article
- Oxidative Stress in Treatment-Resistant and Refractory Depression: A Hidden Therapeutic Target?Molecular neurobiology · 2026Review
- Relationship Between the Duration of Intravenous Ketamine Anesthesia and Postoperative Oxidative Stress and Inflammatory Response in Rats.International journal of molecular sciences · 2025Article
- A Preliminary Approach to Oral Low-Dose Ketamine Self-Administration in Mice (Current issues in molecular biology · 2025Article
- The Role of Intravenous Anesthetics for Neuro: Protection or Toxicity?Neuroscience bulletin · 2025Review
- Altered lipid profiles in the prefrontal cortex are associated with neuroinflammation after severe burn injury.Frontiers in immunology · 2025Article
- NMDA receptors antagonists alleviated the acute phase of traumatic brain injury.Iranian journal of basic medical sciences · 2025Article
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- The Antinociceptive Role of Nrf2 in Neuropathic Pain: From Mechanisms to Clinical Perspectives.Pharmaceutics · 2024Review
- Intranasal delivery of mitochondria targeted neuroprotective compounds for traumatic brain injury: screening based on pharmacological and physiological properties.Journal of translational medicine · 2024Review
- Broadening horizons: ferroptosis as a new target for traumatic brain injury.Burns & trauma · 2024Review
- Hippocampus protection from apoptosis by Baicalin in a LiCl-pilocarpine-induced rat status epilepticus model through autophagy activation.World journal of psychiatry · 2023Article
- Effects of a Subanesthetic Ketamine Infusion on Inflammatory and Behavioral Outcomes after Closed Head Injury in Rats.Bioengineering (Basel, Switzerland) · 2023Article
- Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Article
- Sex-based differences of antioxidant enzyme nanoparticle effects following traumatic brain injury.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Pathological changes in the brain after peripheral burns.Burns & trauma · 2023Review
- Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side.International journal of molecular sciences · 2022Review
- Ketamine administration ameliorates anesthesia and surgery-induced cognitive dysfunction via activation of TRPV4 channel opening.Experimental and therapeutic medicine · 2022Article
- Effects of an intravenous ketamine infusion on inflammatory cytokine levels in male and female Sprague-Dawley rats.Journal of neuroinflammation · 2022Article
Corrections and comments
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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
backgroundKetamine can act as a multifunctional neuroprotective agent by inhibiting oxidative stress, cellular dysfunction, and apoptosis. Although it has been proven to be effective in various neurologic disorders, the mechanism of the treatment of traumatic brain injury (TBI) is not fully understood. The aim of this study was to investigate the neuroprotective function of ketamine in models of TBI and the potential role of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this putative protective effect. MATERIALS AND
methodsWild-type male mice were randomly assigned to five groups: Sham group, Sham + ketamine group, TBI group, TBI + vehicle group, and TBI + ketamine group. Marmarou's weight drop model in mice was used to induce TBI, after which either ketamine or vehicle was administered via intraperitoneal injection. After 24 h, the brain samples were collected for analysis.
resultsKetamine significantly ameliorated secondary brain injury induced by TBI, including neurological deficits, brain water content, and neuronal apoptosis. In addition, the levels of malondialdehyde (MDA), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were restored by the ketamine treatment. Western blotting and immunohistochemistry showed that ketamine significantly increased the level of Nrf2. Furthermore, administration of ketamine also induced the expression of Nrf2 pathway-related downstream factors, including hemeoxygenase-1 and quinine oxidoreductase-1, at the pre- and post-transcriptional levels.
conclusionKetamine exhibits neuroprotective effects by attenuating oxidative stress and apoptosis after TBI. Therefore, ketamine could be an effective therapeutic agent for the treatment of TBI.
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