2008Di-Si Junyi Daxue xuebaoRequires access

Influence of NF-κB on COX-2 expression in substantia nigra of mouse models of Parkinson's disease induced by MPTP

Yu Zhang

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Abstract

AIM:To investigate the effect of NF-κB on the expression of cyclooxygenase-2(COX-2)in substantia nigra(SN)of the mouse models of Parkinson's disease(PD)induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)and investigate the influence of ginsenoside Rg1 on NF-κB to further explore the possible mechanism of the dopaminergic(DA)neuron death in PD.METHODS:C57BL/6N mice were administrated with MPTP to produce subacute PD models.PD mice were observed in behavioral changes.Immunohistochemistry and Western Blot for tyrosine hydroxylase(TH),COX-2,prostaglandine 2(PGE2)and NF-κB were used to observe the changes of positive cell number in the midbrain and the changes after treated with ginsenoside Rg1.RESULTS:Compared with the mice in control group,the model mice represented the typical symptoms of PD.The numbers of NF-κB(34.6±5.6),COX-2(28.2±5.1),PGE2(36.1±4.2)immunoreactive cells were significantly increased in SN area at 24 h after the 5 th injection of 30 mg/kg MPTP(P0.01)compared with the numbers of NF-κB(2.5±0.8),COX-2(1.0±0.3),PGE2(3.2±0.4)immunoreactive cells in control group.The number of TH-positive neurons in model group was distinctly reduced by about 60%(P0.01).In ginsenoside Rg1 treated group,the numbers of NF-κB(4.9±2.1),COX-2(1.9±0.7),PGE2(4.6±0.3)positive cells were reduced obviously as compared with the model group(P0.01),and the number of TH-positive neurons in SN was only decreased by 32%(P0.01 vs control group).CONCLUSION:NF-κB may play an important role in mediating COX-2 expression in SN in the early stage of the MPTP-induced subacute PD,and ginsenoside Rg1 may influence the expression of NF-κB and protect the DA neurons in PD.

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AIM:To investigate the effect of NF-κB on the expression of cyclooxygenase-2(COX-2)in substantia nigra(SN)of the mouse models of Parkinson's disease(PD)induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)and investigate the influence of ginsenoside Rg1 on NF-κB to further explore the possible mechanism of the dopaminergic(DA)neuron death in PD.METHODS:C57BL/6N mice were administrated with MPTP to produce subacute PD models.PD mice were observed in behavioral changes.Immunohistochemistry and Western Blot for tyrosine hydroxylase(TH),COX-2,prostaglandine 2(PGE2)and NF-κB were used to observe the changes of positive cell number in the midbrain and the changes after treated with ginsenoside Rg1.RESULTS:Compared with the mice in control group,the model mice represented the typical symptoms of PD.The numbers of NF-κB(34.6±5.6),COX-2(28.2±5.1),PGE2(36.1±4.2)immunoreactive cells were significantly increased in SN area at 24 h after the 5 th injection of 30 mg/kg MPTP(P0.01)compared with the numbers of NF-κB(2.5±0.8),COX-2(1.0±0.3),PGE2(3.2±0.4)immunoreactive cells in control group.The number of TH-positive neurons in model group was distinctly reduced by about 60%(P0.01).In ginsenoside Rg1 treated group,the numbers of NF-κB(4.9±2.1),COX-2(1.9±0.7),PGE2(4.6±0.3)positive cells were reduced obviously as compared with the model group(P0.01),and the number of TH-positive neurons in SN was only decreased by 32%(P0.01 vs control group).CONCLUSION:NF-κB may play an important role in mediating COX-2 expression in SN in the early stage of the MPTP-induced subacute PD,and ginsenoside Rg1 may influence the expression of NF-κB and protect the DA neurons in PD.

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Available abstract

AIM:To investigate the effect of NF-κB on the expression of cyclooxygenase-2(COX-2)in substantia nigra(SN)of the mouse models of Parkinson's disease(PD)induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)and investigate the influence of ginsenoside Rg1 on NF-κB to further explore the possible mechanism of the dopaminergic(DA)neuron death in PD.METHODS:C57BL/6N mice were administrated with MPTP to produce subacute PD models.PD mice were observed in behavioral changes.Immunohistochemistry and Western Blot for tyrosine hydroxylase(TH),COX-2,prostaglandine 2(PGE2)and NF-κB were used to observe the changes of positive cell number in the midbrain and the changes after treated with ginsenoside Rg1.RESULTS:Compared with the mice in control group,the model mice represented the typical symptoms of PD.The numbers of NF-κB(34.6±5.6),COX-2(28.2±5.1),PGE2(36.1±4.2)immunoreactive cells were significantly increased in SN area at 24 h after the 5 th injection of 30 mg/kg MPTP(P0.01)compared with the numbers of NF-κB(2.5±0.8),COX-2(1.0±0.3),PGE2(3.2±0.4)immunoreactive cells in control group.The number of TH-positive neurons in model group was distinctly reduced by about 60%(P0.01).In ginsenoside Rg1 treated group,the numbers of NF-κB(4.9±2.1),COX-2(1.9±0.7),PGE2(4.6±0.3)positive cells were reduced obviously as compared with the model group(P0.01),and the number of TH-positive neurons in SN was only decreased by 32%(P0.01 vs control group).CONCLUSION:NF-κB may play an important role in mediating COX-2 expression in SN in the early stage of the MPTP-induced subacute PD,and ginsenoside Rg1 may influence the expression of NF-κB and protect the DA neurons in PD.

Key concepts: MPTP, Substantia nigra, Tyrosine hydroxylase, Parkinson's disease, Dopaminergic, Immunohistochemistry, Internal medicine, Endocrinology

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