ArticleMolecular medicine reports2018
Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- The Role of Intravenous Anesthetics for Neuro: Protection or Toxicity?Neuroscience bulletin · 2025Review
- Progress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.Brain and behavior · 2024Review
- Elevated Expression of HSP72 in the Prefrontal Cortex and Hippocampus of Rats Subjected to Chronic Mild Stress and Treated with Imipramine.International journal of molecular sciences · 2023Article
- HSP70 attenuates neuronal necroptosis through the HSP90α-RIPK3 pathway following neuronal trauma.Molecular biology reports · 2023Article
- Article
- Satureja khuzistanica Jamzad essential oil and pure carvacrol attenuate TBI-induced inflammation and apoptosis via NF-κB and caspase-3 regulation in the male rat brain.Scientific reports · 2023Article
- Article
- Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies.Frontiers in neurology · 2023Review
- Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side.International journal of molecular sciences · 2022Review
- Spatial and temporal dynamics of HDACs class IIa following mild traumatic brain injury in adult rats.Molecular psychiatry · 2022Article
- The neuroprotective effect of dexmedetomidine and its mechanism.Frontiers in pharmacology · 2022Review
- The heat shock response and small molecule regulators.European journal of medicinal chemistry · 2021Review
- Synergistic effects of brain injury and aging: common mechanisms of proteostatic dysfunction.Trends in neurosciences · 2021Review
- Edaravone alleviated propofol-induced neural injury in developing rats by BDNF/TrkB pathway.Journal of cellular and molecular medicine · 2021Article
- HSP70 expression before and after treatment and its clinical value in patients with acute angle-closure glaucoma.Experimental and therapeutic medicine · 2021Article
- T Cell-Mediated Autoimmunity in Glaucoma Neurodegeneration.Frontiers in immunology · 2021Review
- Dexmedetomidine inhibits the PSD95-NMDA receptor interaction to promote functional recovery following traumatic brain injury.Experimental and therapeutic medicine · 2021Article
- Novel Synthetic and Natural Therapies for Traumatic Brain Injury.Current neuropharmacology · 2021Review
- Effects of local dexmedetomidine administration on the neurotoxicity of ropivacaine for sciatic nerve block in rats.Molecular medicine reports · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in the hippocampus. A total of 90 adult male Sprague‑Dawley rats were randomly assigned into 3 groups (n=30/group): Sham, TBI and Dex groups. The rat models of TBI were established using a modified weight‑drop device and Dex (15 µg/kg) was intravenously administered immediately following TBI. The brain edema and neurological function outcomes of TBI were assessed using wet‑dry weight analysis and the Neurological Severity Score method. The expression levels of B‑cell lymphoma‑2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) in the rat hippocampus were evaluated using immunohistochemical staining and western blot analysis. The protein levels of HSP70 in the hippocampal region were analyzed using western blot analysis. The results of the present study revealed that administration of Dex post‑TBI improved brain edema and neurological outcomes, due to the attenuation of the TBI‑induced reduction of Bax expression and increase of Bcl‑2 and HSP70 expression. In conclusion, the results of the present study suggested that administration of Dex may serve as a neuroprotective agent against brain injury, at least partially via the inhibition of neuronal apoptosis and upregulation of HSP70 expression in the hippocampus.
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