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Protective effect of mild hypothermia on oxygen-glucose deprivation injury in rat hippocampal neurons after hypoxia

机译:亚低温对缺氧后大鼠海马神经元缺氧葡萄糖剥夺的保护作用

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摘要

The present study aimed to establish an oxygen-glucose deprivation (OGD) model of ischemic and hypoxic cerebral neurons to investigate the protective effect of mild hypothermia on neuronal OGD and its mechanisms. OGD injury was significantly mitigated in cells with 24 h of mild hypothermia compared with cells without mild hypothermia; cell morphology improved, the lactic acid dehydrogenase (LDH) release rate was decreased, cytoactivity was increased and the neuronal apoptotic rate was decreased. By contrast, no significant improvement in injury was observed after 6 h of mild hypothermia. This suggests that mild hypothermia treatment following OGD is effective only when implemented for 24 h. Additionally, the caspase-3 activity of neurons increased following OGD, which was positively associated with the neuronal apoptotic rate. However, the caspase-3 activity after 24 h of mild hypothermia was reduced. Simultaneously, the neuronal apoptotic rate was decreased, suggesting that mild hypothermia may inhibit neuronal apoptosis by reducing caspase-3 activity. Therefore, reducing caspase-3 activity potentially constitutes one of the protective mechanisms of mild hypothermia in neuronal OGD.
机译:本研究旨在建立缺血性和缺氧性脑神经元的氧葡萄糖剥夺(OGD)模型,以研究轻度低温对神经元OGD的保护作用及其机制。与没有轻度低温的细胞相比,轻度低温24 h的细胞OGD损伤明显减轻。细胞形态改善,乳酸脱氢酶(LDH)释放速率降低,细胞活性增加,神经元凋亡率降低。相比之下,轻度亚低温6小时后未观察到损伤的明显改善。这表明OGD后进行温和的低温治疗仅在实施24小时后才有效。另外,OGD后神经元的caspase-3活性增加,这与神经元凋亡率呈正相关。但是,轻度低温24小时后caspase-3活性降低。同时,神经元的凋亡率降低,表明轻度的低温可能通过降低caspase-3活性来抑制神经元的凋亡。因此,降低caspase-3活性可能构成了神经元OGD中亚低温的保护机制之一。

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