2013•Zhongguo bingli shengli zazhiRequires access

Mild hypothermia protects against injury of rat hippocampal neurons induced by oxygen-glucose deprivation

Longyuan Jiang

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Abstract

AIM: To study the protective effect of mild hypothermia(31 ~32 °C) on rat hippocampal neurons against oxygen-glucose deprivation(OGD)-induced injury and its possible mechanisms.METHODS: An OGD experimental model of rat hippocampal neurons in vitro was established to simulate cerebral ischemic-hypoxic injury.The rat hippocampal neurons were randomly divided into 4 groups: control group,mild hypothermia group,OGD group and mild hypothermia + OGD group.The cell morphology was observed under light and electron microscopes.The neuronal apoptosis was detected by flow cytometry.The activity of caspase-3 in the cytoplasm was measured by colorimetry.RESULTS: The neuronal injury was apparent after OGD,with a great increase in apoptotic rate(P 0.01).Compared with OGD group,the morphology of neuronal injury in mild hypothermia + OGD group was attenuated,and the neuronal apoptotic rate and the activity of caspase-3 in the cytoplasm decreased.The activity of caspase-3 in the cytoplasm increased after OGD,and was positively correlated with the neuronal apoptotic rate(r = 0.823,P 0.05).The activity of caspase-3 in the cytoplasm also increased after mild hypothermia and OGD,and was also positively correlated with the neuronal apoptotic rate(r = 0.841,P 0.05).CONCLUSION: OGD can increase caspase-3 activity in the neuronal cytoplasm and induce neuronal apoptosis.Restraint on caspase-3 activity in the neuronal cytoplasm may be the mechanism by which mild hypothermia protects against neuronal injury induced by OGD.

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AIM: To study the protective effect of mild hypothermia(31 ~32 °C) on rat hippocampal neurons against oxygen-glucose deprivation(OGD)-induced injury and its possible mechanisms.METHODS: An OGD experimental model of rat hippocampal neurons in vitro was established to simulate cerebral ischemic-hypoxic injury.The rat hippocampal neurons were randomly divided into 4 groups: control group,mild hypothermia group,OGD group and mild hypothermia + OGD group.The cell morphology was observed under light and electron microscopes.The neuronal apoptosis was detected by flow cytometry.The activity of caspase-3 in the cytoplasm was measured by colorimetry.RESULTS: The neuronal injury was apparent after OGD,with a great increase in apoptotic rate(P 0.01).Compared with OGD group,the morphology of neuronal injury in mild hypothermia + OGD group was attenuated,and the neuronal apoptotic rate and the activity of caspase-3 in the cytoplasm decreased.The activity of caspase-3 in the cytoplasm increased after OGD,and was positively correlated with the neuronal apoptotic rate(r = 0.823,P 0.05).The activity of caspase-3 in the cytoplasm also increased after mild hypothermia and OGD,and was also positively correlated with the neuronal apoptotic rate(r = 0.841,P 0.05).CONCLUSION: OGD can increase caspase-3 activity in the neuronal cytoplasm and induce neuronal apoptosis.Restraint on caspase-3 activity in the neuronal cytoplasm may be the mechanism by which mild hypothermia protects against neuronal injury induced by OGD.

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Available abstract

AIM: To study the protective effect of mild hypothermia(31 ~32 °C) on rat hippocampal neurons against oxygen-glucose deprivation(OGD)-induced injury and its possible mechanisms.METHODS: An OGD experimental model of rat hippocampal neurons in vitro was established to simulate cerebral ischemic-hypoxic injury.The rat hippocampal neurons were randomly divided into 4 groups: control group,mild hypothermia group,OGD group and mild hypothermia + OGD group.The cell morphology was observed under light and electron microscopes.The neuronal apoptosis was detected by flow cytometry.The activity of caspase-3 in the cytoplasm was measured by colorimetry.RESULTS: The neuronal injury was apparent after OGD,with a great increase in apoptotic rate(P 0.01).Compared with OGD group,the morphology of neuronal injury in mild hypothermia + OGD group was attenuated,and the neuronal apoptotic rate and the activity of caspase-3 in the cytoplasm decreased.The activity of caspase-3 in the cytoplasm increased after OGD,and was positively correlated with the neuronal apoptotic rate(r = 0.823,P 0.05).The activity of caspase-3 in the cytoplasm also increased after mild hypothermia and OGD,and was also positively correlated with the neuronal apoptotic rate(r = 0.841,P 0.05).CONCLUSION: OGD can increase caspase-3 activity in the neuronal cytoplasm and induce neuronal apoptosis.Restraint on caspase-3 activity in the neuronal cytoplasm may be the mechanism by which mild hypothermia protects against neuronal injury induced by OGD.

Key concepts: Hippocampal formation, Apoptosis, Hypothermia, Cytoplasm, Biology, Caspase 3, Internal medicine, Endocrinology

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