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Cellular Mechanisms of Spatial Memory Recovery via Hyperbaric Oxygen Therapy in Experimental TBI: A Review Jaslindo, Lieka Nugrahi; Ibrahim, Nurhadi
Biomedical Journal of Indonesia Vol. 11 No. 3 (2025): Vol 11, No 3, 2025
Publisher : Fakultas Kedokteran Universitas Sriwijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32539/bji.v11i3.267

Abstract

Traumatic Brain Injury (TBI) impairs spatial memory, affects individuals' quality of life, and increases disability and mortality rates. Hyperbaric Oxygen Therapy (HBOT), which delivers nearly 100% oxygen in a pressurised environment, has a potential intervention to ameliorate these cognitive deficits. This narrative review presents evidence from animal studies demonstrating the efficacy of HBOT in enhancing spatial memory in rats with TBI. Specifically, we present evidence that HBOT increases levels of Brain-Derived Neurotrophic Factor (BDNF) and activates the Hypoxia-Inducible Factor 1-alpha (HIF-1α) pathway. These molecular changes foster neuroplasticity and reduce oxidative stress, thereby promoting the repair and growth of dendritic spines and decreasing Reactive Oxygen Species (ROS) levels to prevent neuronal death. By elucidating these mechanisms, this review shows how HBOT contributes to spatial memory recovery in TBI, suggesting a promising therapeutic avenue that need further clinical exploration to refine treatment protocols and evaluate its applicability in human TBI recovery.
Vitamin D and Traumatic Brain Injury: A Systematic Review of Preclinical Evidence Jaslindo, Lieka Nugrahi; Sari, Widia; Dhuha, Alief; Handayani, Kurnia Maidarmi; Khudri, Ghaniyyatul Nugrahi; Maribeth, Annisa Lidra
Health and Medical Journal Vol. 8 No. 1 (2026): HEME January 2026
Publisher : Universitas Baiturrahmah

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33854/heme.v8i1.2096

Abstract

Traumativ Brain Injury (TBI) triggers multiple secondary injury processes, such as inflammation, oxidative stress, apoptosis, BBB disruption, and impaired autophagy. These mechanisms contribute to progressive neuronal damage and functional decline. Vitamin D has emerged as a potential multi-target neuroprotective agent due to its regulatory roles in immune signaling, oxidative balance, neuronal survival, and autophagy pathways. This systematic review synthesized preclinical evidence evaluating the effects of Vitamin D supplementation in animal models of TBI. A comprehensive search of PubMed, OVID, and ProQuest identified six eligible studies. Across diverse dosing regimens and formulations, Vitamin D consistently improved key TBI outcomes. Reported benefits included reduced apoptosis, decreased neuroinflammation, attenuation of oxidative stress, preservation of BBB integrity, restoration of autophagy flux, and enhanced cognitive performance. Mechanistically, Vitamin D influenced several pathways, including Nrf2 activation, TLR4/MyD88/NF-κB suppression, mTOR and TRPM2 normalization, and improved microglial polarization. Although methodological quality varied, most studies demonstrated moderate rigor and supported the neuroprotective actions of Vitamin D. Heterogeneity in injury models, dosing strategies, and outcome measures limits direct comparison and highlights the need for standardized experimental approaches. Overall, current preclinical evidence indicates that Vitamin D confers robust neuroprotection following TBI. Further studies examining its mechanistic pathways, optimal therapeutic windows, and translational potential are warranted to inform future clinical applications.