2009Journal of Zhengzhou UniversityRequires access

Expression of HMGB1 and NF-κB in cultured neurons of rat after hypoxia/reoxygenation

Wang Man-li

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Abstract

Aim:To explore the effects of HMGB1 and NF-κB on neuronal apoptosis caused by ischemia-reperfusion injury.Methods:The cortical neurons cultured for 7 days were randomly divided into A(normal control group),B[hypoxia/reoxygenation(H/R) alone],C(treatment with rHMGB1,and without H/R),D(pretreatment with PTDC and H/R) groups.The expressions of HMGB1,NF-κB were tested by immunocytochemical technique,cell survival rate was detected by MTT colorimetry,and the apoptotic was detected by TUNEL,after reoxygenation or after finishing treatment with rHMGB1 0,1,3,6,12,24 h.Results:Compared with those of Group A,in Group B and C,the expressions of HMGB1 and NF-κB in neurons were stronger,and the apoptotic neuron was more obviously,the cell survival rate decreased(P0.05).Compared with those of Group B,the expressions of HMGB1 and NF-κB,and the apoptotic neurons quantity were lower and the survival rate increased in Group D(P0.05).The expressions of HMGB1 and NF-κB were both positively correlated to the apoptosis,and HMGB1 had positive correlation with NF-κB in Group B(r was 0.660,0.774,0.737,respectively,P0.05).Conclusion:IRI could increase the expressions of HMGB1 and NF-κB of neurons.HMGB1 and NF-κB may be induced mutually in neurons,and related to neurons apoptosis.

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Aim:To explore the effects of HMGB1 and NF-κB on neuronal apoptosis caused by ischemia-reperfusion injury.Methods:The cortical neurons cultured for 7 days were randomly divided into A(normal control group),B[hypoxia/reoxygenation(H/R) alone],C(treatment with rHMGB1,and without H/R),D(pretreatment with PTDC and H/R) groups.The expressions of HMGB1,NF-κB were tested by immunocytochemical technique,cell survival rate was detected by MTT colorimetry,and the apoptotic was detected by TUNEL,after reoxygenation or after finishing treatment with rHMGB1 0,1,3,6,12,24 h.Results:Compared with those of Group A,in Group B and C,the expressions of HMGB1 and NF-κB in neurons were stronger,and the apoptotic neuron was more obviously,the cell survival rate decreased(P0.05).Compared with those of Group B,the expressions of HMGB1 and NF-κB,and the apoptotic neurons quantity were lower and the survival rate increased in Group D(P0.05).The expressions of HMGB1 and NF-κB were both positively correlated to the apoptosis,and HMGB1 had positive correlation with NF-κB in Group B(r was 0.660,0.774,0.737,respectively,P0.05).Conclusion:IRI could increase the expressions of HMGB1 and NF-κB of neurons.HMGB1 and NF-κB may be induced mutually in neurons,and related to neurons apoptosis.

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Available abstract

Aim:To explore the effects of HMGB1 and NF-κB on neuronal apoptosis caused by ischemia-reperfusion injury.Methods:The cortical neurons cultured for 7 days were randomly divided into A(normal control group),B[hypoxia/reoxygenation(H/R) alone],C(treatment with rHMGB1,and without H/R),D(pretreatment with PTDC and H/R) groups.The expressions of HMGB1,NF-κB were tested by immunocytochemical technique,cell survival rate was detected by MTT colorimetry,and the apoptotic was detected by TUNEL,after reoxygenation or after finishing treatment with rHMGB1 0,1,3,6,12,24 h.Results:Compared with those of Group A,in Group B and C,the expressions of HMGB1 and NF-κB in neurons were stronger,and the apoptotic neuron was more obviously,the cell survival rate decreased(P0.05).Compared with those of Group B,the expressions of HMGB1 and NF-κB,and the apoptotic neurons quantity were lower and the survival rate increased in Group D(P0.05).The expressions of HMGB1 and NF-κB were both positively correlated to the apoptosis,and HMGB1 had positive correlation with NF-κB in Group B(r was 0.660,0.774,0.737,respectively,P0.05).Conclusion:IRI could increase the expressions of HMGB1 and NF-κB of neurons.HMGB1 and NF-κB may be induced mutually in neurons,and related to neurons apoptosis.

Key concepts: Apoptosis, HMGB1, TUNEL assay, Hypoxia (environmental), NF-κB, Neuron, Cortical neurons, Andrology

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