2015•Academic Journal of Second Military Medical UniversityRequires access

Activation of α7 nicotinic acetylcholine receptor alleviates cerebral cortical neuron injury induced by oxygen-glucose deprivation

Xin Ru-jua

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Abstract

Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.

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Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.

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Available abstract

Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.

Key concepts: Apoptosis, Reactive oxygen species, Lactate dehydrogenase, Viability assay, Cell, Oxidative stress, Receptor, Acetylcholine

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