ArticleNeuropsychiatric disease and treatment2023
The Protective Role and Mechanism of Mild Therapeutic Hypothermia Protection on Brain Cells.
Article in Neuropsychiatric disease and treatment, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Head mild hypothermia treatment after successful mechanical thrombectomy in anterior circulation large-vessel occlusion acute cerebral infarction.European journal of medical research · 2026Article
- Mild hypothermia regulates neuronal inflammation and oxidative stress through HSP70 to alleviate brachial plexus injury.IBRO neuroscience reports · 2025Article
- Advancements in the application of multimodal monitoring and machine learning for the development of personalized therapeutic strategies in traumatic brain injury.Frontiers in human neuroscience · 2025Review
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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
Background: Moderate therapeutic hypothermia is protective against several cellular stressors. However, the mechanisms behind this protection are not entirely known. In the current investigation, we investigated that therapeutic hypothermia at 33°C administered following peroxide-induced oxidative stress might protect human oligodendroglioma cells using an in vitro model. Methods and Results: Tert-butyl peroxide treatment for one hour significantly increased cell apoptosis and suppressed cell viability. In the range of 50-1000 M tert-butyl peroxide, this cell death was dose-dependent. MTT assay and cell apoptosis assay were applied to analyze cell viability/death at 24 hours after peroxide-induced stress. Therapeutic hypothermia at 33°C delivered for two hours after peroxide exposure significantly increased cell viability and suppressed cell death. Even 15 minutes after peroxide washout when delayed hypothermia was used, this protection was still apparent. Three FDA-approved antioxidants (Tempol, EUK134, and Edaravone at 100 M) were added immediately after tert-butyl peroxide, followed by hypothermia treatment. These three antioxidants greatly increased cell viability and cell apoptosis. RT-qPCR was applied to determine the effects of hypothermia treatment on the expression of caspase-3 and -8 as well as tumor necrosis factor-alpha (TNF-α). Therapeutic hypothermia significantly downregulated these three factors. Conclusion: Overall, these findings confirmed that hypothermia and antioxidants quenching reactive oxygen species may lower mitochondrial oxidative stress and/or apoptotic pathways. Further investigation are needed to investigate the role of hypothermia in other cell models.
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