ArticleInternational journal of medical sciences2025
Hyperbaric oxygen therapy attenuates brain radiation-induced cognitive deficits in rats.
Article in International journal of medical sciences, 2025. 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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Who cites it
3 citing papers in PubMed.
- Hyperbaric Oxygen Therapy for Cognitive Impairment Resulting from Neurological Disorders: Mechanisms of Action and Application Advances.International journal of medical sciences · 2026Review
- Hyperbaric oxygen protects against periodontal bone loss by modulating inflammation and bone remodeling via RANKL/OPG expression in ligature-induced periodontitis.International journal of medical sciences · 2026Article
- Heat acclimation prevents neurobehavioral and physiological disorders in mice exposed to chronic aircraft noise.Physiological reports · 2025Article
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Authors and funding
10 authors.
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Abstract
Effective therapies for cognitive impairments induced by brain irradiation are currently lacking. This study investigated the therapeutic potential of hyperbaric oxygen therapy (HBOT) for radiation-induced brain injury in a randomized controlled experimental model using adult male Wistar rats. Adult male Wistar rats were divided into four experimental groups: 0 Gy whole brain radiotherapy (WBRT) with normal baric air (NBA) treatment, 0 Gy WBRT with HBOT, 10 Gy WBRT with NBA, and 10 Gy WBRT with HBOT. Behavioral tests and histochemical analyses were conducted four weeks post-WBRT to assess cognitive function, hippocampal microgliosis, apoptosis, and lipid peroxidation. Compared with the rats with 0 Gy WBRT on 28 days, the rats with 10 Gy WBRT on 28 days had significantly higher severity of spatial learning and memory dysfunction and hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. HBOT significantly prevented and reversed WBRT-induced cognitive deficits, hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. In addition, HBOT prevented and reversed the increased apoptosis among newborn neural stem cells and neuroblasts caused by 10 Gy WBRT on 7 days. The findings suggest that WBRT disrupts neurogenesis and enhance microgliosis, apoptosis of neuronal progenitors, and lipid peroxidation in the dentate gyrus, potentially leading to cognitive deficits and neuronal death. HBOT may offer a protective effect against these cognitive impairments and their underlying mechanisms in adult male rats following WBRT.
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