Zhou Quanming, Wu Shejuan, Zhu Hongzai
Department of Neurosurgery, Affiliated Hospital of Putian University, 351100 Putian, Fujian, China.
Discov Med. 2025 May;37(196):850-861. doi: 10.24976/Discov.Med.202537196.75.
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.
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 () in HBO therapy, was silenced or overexpressed. After transfection, the cellular functions and the levels of related factors were re-examined.
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 ( < 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 ( < 0.01). 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 ( < 0.05).
HBO inhibits TNFR1 expression to down-regulate NO content in TBI in an model.
高压氧（HBO）疗法可能是创伤性脑损伤（TBI）的一种治疗选择。本研究旨在探究HBO治疗TBI的机制。
将从健康新生大鼠皮质分离的神经元和星形胶质细胞共培养，建立TBI模型，并在HBO条件下培养细胞。通过免疫荧光评估神经元/星形胶质细胞共培养物中的神经元/星形胶质细胞活力和谷氨酸转运体-1（GLT-1）表达。使用定量实时聚合酶链反应（qRT-PCR）、比色法和蛋白质印迹法检测神经元/星形胶质细胞共培养物中的肿瘤坏死因子（TNF）-α/肿瘤坏死因子受体1（TNFR1）/一氧化氮（NO）/神经元型一氧化氮合酶（nNOS）/白细胞介素（IL）-1β/诱导型一氧化氮合酶（iNOS）/GLT-1水平。为了确定靶基因TNF受体1（）在HBO治疗中的关键作用，对其进行沉默或过表达。转染后，重新检测细胞功能和相关因子水平。
HBO（2个绝对大气压（ATA），持续30/60分钟）减弱了TBI诱导的对神经元活力降低、星形胶质细胞活力增加、TNF-α、IL-1β、NO、nNOS、iNOS和TNFR1水平上调、GLT-1水平下调以及神经元/星形胶质细胞共培养物中GLT-1阳性星形胶质细胞减少的影响（<0.05）。TNFR1敲低和HBO（2 ATA，持续60分钟）增强了TBI诱导的神经元/星形胶质细胞共培养物中的神经元活力，降低了星形胶质细胞活力，并下调了TNF-α、IL-1β、NO、nNOS、iNOS和TNFR1水平（<0.01）。过表达逆转了HBO在TBI诱导的神经元/星形胶质细胞共培养物中的上述作用。HBO（2 ATA，持续60分钟）上调了TBI诱导的神经元/星形胶质细胞共培养物中的GLT-1水平（<0.05）。
在模型中，HBO通过抑制TNFR1表达来下调TBI中的NO含量。
