ArticleNeuropsychiatric disease and treatment2018
Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway.
Article in Neuropsychiatric disease and treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 26 citations in OpenAlex.
- Remimazolam alleviates cerebral ischemia-reperfusion injury of rats by inhibiting NF-κB/NLRP3 inflammasome pyroptosis.Scientific reports · 2025Article
- From neurotoxicity to neuroprotection: Rethinking GABACell biology and toxicology · 2025Review
- Study on the mechanism of Dexmedetomidine's effect on postoperative cognitive dysfunction in elderly people.Frontiers in physiology · 2025Review
- Dexmedetomidine improves the circulatory dysfunction of the glymphatic system induced by sevoflurane through the PI3K/AKT/ΔFosB/AQP4 pathway in young mice.Cell death & disease · 2024Article
- Anesthesia, Anesthetics, and Postoperative Cognitive Dysfunction in Elderly Patients.Current medical science · 2024Review
- Dexmedetomidine Pretreatment of Neuronal Cells Has Protective Effect Against Cell Death During Oxygen-glucose Deprivation/Reoxygenation, Based on IGF-1 Production.Juntendo Iji zasshi = Juntendo medical journal · 2024Article
- Role of ferroptosis in hypoxic preconditioning to reduce propofol neurotoxicity.Frontiers in pharmacology · 2023Article
- A Review of the Biological Mechanisms of Dexmedetomidine for Postoperative Neurocognitive Disorders.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Dexmedetomidine reduces propofol-induced hippocampal neuron injury by modulating the miR-377-5p/Arc pathway.BMC pharmacology & toxicology · 2022Article
- Dexmedetomidine does not compromise neuronal viability, synaptic connectivity, learning and memory in a rodent model.Scientific reports · 2021Article
- Edaravone alleviated propofol-induced neural injury in developing rats by BDNF/TrkB pathway.Journal of cellular and molecular medicine · 2021Article
- Neuroprotection of the Developing Brain by Dexmedetomidine Is Mediated by Attenuating Single Propofol-induced Hippocampal Apoptosis and Synaptic Plasticity Deficits.Experimental neurobiology · 2020Article
- Dexmedetomidine attenuates the neurotoxicity of propofol toward primary hippocampal neurons in vitro via Erk1/2/CREB/BDNF signaling pathways.Drug design, development and therapy · 2019Article
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9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPropofol induces short- and long-term neurotoxicity. Our previous study showed that dexmedetomidine (Dex) can attenuate the propofol-induced acute neurotoxicity in rodents by enhancing the PI3K/Akt signaling. However, whether treatment of young rats with Dex could protect them from long-term neurotoxicity induced by propofol is unclear. MATERIALS AND
methodsSeven-day-old male Sprague Dawley rats were randomized and injected intraperitoneally with saline (100 μL, NS), propofol (100 mg/kg), Dex (75 μg/kg), propofol (100 mg/kg) plus Dex (25, 50 or 75 μg/kg), 10% dimethyl sulfoxide (DMSO, 100 μL) or TDZD-8 (a GSK3β inhibitor, 1 mg/kg), or intracerebroventricularly with DMSO (5 μL) or LY294002 (a PI3K inhibitor, 25 μg/5 μL DMSO). Other rats in the experimental group were injected with the same doses of propofol, Dex and LY294002 or TDZD-8. All the rats were monitored until they were 9 weeks old. Their spatial learning and memory were tested by Morris water maze. The neuronal apoptosis, expression of PSD
resultsCompared with the NS control group, young rats injected with intralipid, Dex, TDZD-8, LY294002 or DMSO alone did not show any significant change as they aged. Propofol significantly increased the escape latency time, hippocampal neuroapoptosis and synaptic ultrastructural changes but decreased the relative levels of PSD
conclusionOur results indicated that the pretreatment of young rats with Dex attenuated the propofol-induced long-term neurotoxicity in their developing hippocampus by enhancing the PI3K/Akt signaling.
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