Discovery medicine · 2025
Mechanism Underlying Hyperbaric Oxygen's Effect on Nitric Oxide in an in Vitro Model of Traumatic Brain Injury.
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Zhou Quanming, Wu Shejuan, Zhu Hongzai
Аннотация
BACKGROUND: Hyperbaric oxygen (HBO) therapy functions as a possible therapeutic option for traumatic brain injury (TBI). The aim of this study is to detect the mechanism of HBO on TBI.
METHODS: Neurons and astrocytes isolated from healthy neonatal rat cortices were co-cultured, a TBI model was established, and cells were cultured under HBO conditions. Neuron/astrocyte viability and glutamate transporter-1 (GLT-1) expression in neuron/astrocyte co-cultures were assessed by immunofluorescence. Tumor necrosis factor (TNF)-α/tumor necrosis factor receptor 1 (TNFR1)/nitric oxide (NO)/neuronal nitric oxide synthase (nNOS)/interleukin (IL)-1β/inducible nitric oxide synthase (iNOS)/GLT-1 levels in neuron/astrocyte co-cultures were detected using quantitative real-time polymerase chain reaction (qRT-PCR), colorimetry, and western blotting. To identify the key role of the target gene TNF receptor 1 (TNFR1) in HBO therapy, TNFR1 was silenced or overexpressed. After transfection, the cellular functions and the levels of related factors were re-examined.
RESULTS: HBO (2 atmospheric absolute (ATA) for 30/60 min) attenuated the effect of TBI-induced on decrease of neuronal viability, increase of astrocyte viability, up-regulation of TNF-α, IL-1β, NO, nNOS, iNOS, and TNFR1 levels, down-regulation of GLT-1 levels, and reduce of GLT-1-positive astrocytes in neuron/astrocyte co-cultures (p < 0.05). TNFR1 knockdown and HBO (2 ATA for 60 min) enhanced neuronal viability, decreased astrocyte viability, and down-regulated TNF-α, IL-1β, NO, nNOS, iNOS, and TNFR1 levels in TBI-induced neuron/astrocyte co-cultures (p < 0.01). TNFR1 overexpression reversed the above role of HBO in TBI-induced neuron/astrocyte co-cultures. HBO (2 ATA for 60 min) up-regulated GLT-1 levels in TBI-induced neuron/astrocyte co-cultures (p < 0.05).
CONCLUSIONS: HBO inhibits TNFR1 expression to down-regulate NO content in TBI in an in vitro model.
METHODS: Neurons and astrocytes isolated from healthy neonatal rat cortices were co-cultured, a TBI model was established, and cells were cultured under HBO conditions. Neuron/astrocyte viability and glutamate transporter-1 (GLT-1) expression in neuron/astrocyte co-cultures were assessed by immunofluorescence. Tumor necrosis factor (TNF)-α/tumor necrosis factor receptor 1 (TNFR1)/nitric oxide (NO)/neuronal nitric oxide synthase (nNOS)/interleukin (IL)-1β/inducible nitric oxide synthase (iNOS)/GLT-1 levels in neuron/astrocyte co-cultures were detected using quantitative real-time polymerase chain reaction (qRT-PCR), colorimetry, and western blotting. To identify the key role of the target gene TNF receptor 1 (TNFR1) in HBO therapy, TNFR1 was silenced or overexpressed. After transfection, the cellular functions and the levels of related factors were re-examined.
RESULTS: HBO (2 atmospheric absolute (ATA) for 30/60 min) attenuated the effect of TBI-induced on decrease of neuronal viability, increase of astrocyte viability, up-regulation of TNF-α, IL-1β, NO, nNOS, iNOS, and TNFR1 levels, down-regulation of GLT-1 levels, and reduce of GLT-1-positive astrocytes in neuron/astrocyte co-cultures (p < 0.05). TNFR1 knockdown and HBO (2 ATA for 60 min) enhanced neuronal viability, decreased astrocyte viability, and down-regulated TNF-α, IL-1β, NO, nNOS, iNOS, and TNFR1 levels in TBI-induced neuron/astrocyte co-cultures (p < 0.01). TNFR1 overexpression reversed the above role of HBO in TBI-induced neuron/astrocyte co-cultures. HBO (2 ATA for 60 min) up-regulated GLT-1 levels in TBI-induced neuron/astrocyte co-cultures (p < 0.05).
CONCLUSIONS: HBO inhibits TNFR1 expression to down-regulate NO content in TBI in an in vitro model.
Предметные рубрики MeSH
Brain Injuries, TraumaticAnimalsHyperbaric OxygenationRatsNitric OxideAstrocytesCoculture TechniquesNeuronsRats, Sprague-DawleyExcitatory Amino Acid Transporter 2Receptors, Tumor Necrosis Factor, Type INitric Oxide Synthase Type INitric Oxide Synthase Type IICells, CulturedDisease Models, AnimalCell SurvivalTumor Necrosis Factor-alpha