2004Zhongguo kangfu lilun yu shijianRequires access

Study of the influence of Ginsenoside Rb1 on apoptosis of primary cultured neonate rat cerebral cortical neurons caused by hypoxia

Rong Nie

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Abstract

ObjectiveTo investigate the protective mechanism of Ginsenoside Rb1 on apoptosis of primary cultured cerebral cortical neurons caused by hypoxia.MethodsThe anti apoptosis effect of Ginsenoside Rb1 on primary cultured neurons was observed by methods of the primary culture of cerebral neurons of postnatal rats in free serum with neurobasal medium supplied with 2% B27 supplement, trypan blue exclusion, hypoxic culture of neurons, Hoechst 33342 staining and immunocytochemistry.ResultsAt concentrations of 10 μg/ml, 50 μg/ml and 100 μg/ml, the Ginsenoside Rb1 dropped apoptosis rate of cerebral cortical neurons induced by hypoxia (in 100 μg/ml, P0.05), and increased Bcl 2 protein expression (except 10 μg/ml, P0.05) and decreased Bax protein expression (except 10 μg/ml, P0.05— P0.001) in the cerebral cortical neurons induced by hypoxia, improved the ratio of Bcl 2/Bax (except 10 μg/ml, P0.05).ConclusionGinsenoside Rb1 is able to prevent hypoxic neurons from apoptosis in primary cultured cerebral cortical neurons from 50—100 μg/ml. The effect of anti apoptosis is through up regulation of Bcl 2 protein expression and down regulation of Bax 2 protein expression. [

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ObjectiveTo investigate the protective mechanism of Ginsenoside Rb1 on apoptosis of primary cultured cerebral cortical neurons caused by hypoxia.MethodsThe anti apoptosis effect of Ginsenoside Rb1 on primary cultured neurons was observed by methods of the primary culture of cerebral neurons of postnatal rats in free serum with neurobasal medium supplied with 2% B27 supplement, trypan blue exclusion, hypoxic culture of neurons, Hoechst 33342 staining and immunocytochemistry.ResultsAt concentrations of 10 μg/ml, 50 μg/ml and 100 μg/ml, the Ginsenoside Rb1 dropped apoptosis rate of cerebral cortical neurons induced by hypoxia (in 100 μg/ml, P0.05), and increased Bcl 2 protein expression (except 10 μg/ml, P0.05) and decreased Bax protein expression (except 10 μg/ml, P0.05— P0.001) in the cerebral cortical neurons induced by hypoxia, improved the ratio of Bcl 2/Bax (except 10 μg/ml, P0.05).ConclusionGinsenoside Rb1 is able to prevent hypoxic neurons from apoptosis in primary cultured cerebral cortical neurons from 50—100 μg/ml. The effect of anti apoptosis is through up regulation of Bcl 2 protein expression and down regulation of Bax 2 protein expression. [

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Available abstract

ObjectiveTo investigate the protective mechanism of Ginsenoside Rb1 on apoptosis of primary cultured cerebral cortical neurons caused by hypoxia.MethodsThe anti apoptosis effect of Ginsenoside Rb1 on primary cultured neurons was observed by methods of the primary culture of cerebral neurons of postnatal rats in free serum with neurobasal medium supplied with 2% B27 supplement, trypan blue exclusion, hypoxic culture of neurons, Hoechst 33342 staining and immunocytochemistry.ResultsAt concentrations of 10 μg/ml, 50 μg/ml and 100 μg/ml, the Ginsenoside Rb1 dropped apoptosis rate of cerebral cortical neurons induced by hypoxia (in 100 μg/ml, P0.05), and increased Bcl 2 protein expression (except 10 μg/ml, P0.05) and decreased Bax protein expression (except 10 μg/ml, P0.05— P0.001) in the cerebral cortical neurons induced by hypoxia, improved the ratio of Bcl 2/Bax (except 10 μg/ml, P0.05).ConclusionGinsenoside Rb1 is able to prevent hypoxic neurons from apoptosis in primary cultured cerebral cortical neurons from 50—100 μg/ml. The effect of anti apoptosis is through up regulation of Bcl 2 protein expression and down regulation of Bax 2 protein expression. [

Key concepts: Apoptosis, Cortical neurons, Hypoxia (environmental), Trypan blue, Immunocytochemistry, Cerebral cortex, Immunohistochemistry, Neuron

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