2013•Molecular Medicine ReportsOpen access

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

Tianen Zhou, Jun Jiang, MENG ZHANG, Yue Fu, Zhengfei Yang, Longyuan Jiang

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Abstract

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.

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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.

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Available abstract

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.

Key concepts: Hypothermia, Apoptosis, Hippocampal formation, Hypoxia (environmental), Biology, Anesthesia, Neuron, Caspase 3

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