The protective effect of Ginkgo biloba extract on the expression of Bax and Bcl-2 in 6-hydroxydopamine-induced PC12 cells
Xiaoxing Yin
Abstract
Xiaoxing Yin
Abstract
Objective To investigate the protective effect and the causal mechanism of Ginkgo biloba extract(GBE) against PC12 cellular apoptosis induced by 6-hydroxydopamine(6-OHDA).Methods Dopaminergic neuronal injury model was induced by addition of 6-OHDA into PC12 cells cultured in vitro and pretreated at different concentrations of GBE.Cell viability,apoptotic percentage,and the expression of Bax and Bcl-2 were assayed by MTT,FCM and immunoblotting,respectively.Results The livability of PC12 cells treated with 100 μmol/L 6-OHDA for 24 h was lower than that of the control group(P0.01).Compared with the 6-OHDA group,GBE at concentrations of 20 and 40 μg/ml could markedly relieve the toxicity of 6-OHDA on PC12 cells,which suggested that GBE could increase the cellular activity and decrease the percentage of cellular apoptosis.The Bax expression was up-regulated in 6-OHDA groups and Bcl-2 expression was down-regulated(P0.05),compared with the control group.Compared with the 6-OHDA group,the Bax expression was down-regulated and Bcl-2 expression was up-regulated in GBE groups,in a dose-dependent manner(P0.05).The difference had statistic significance.Conclusions As one of the causal mechanisms,GBE has inhibitory effects on the apoptosis of the 6-OHDA-induced PC12 cells by up-regulating Bcl-2 expression and down-regulating Bax expression.
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Objective To investigate the protective effect and the causal mechanism of Ginkgo biloba extract(GBE) against PC12 cellular apoptosis induced by 6-hydroxydopamine(6-OHDA).Methods Dopaminergic neuronal injury model was induced by addition of 6-OHDA into PC12 cells cultured in vitro and pretreated at different concentrations of GBE.Cell viability,apoptotic percentage,and the expression of Bax and Bcl-2 were assayed by MTT,FCM and immunoblotting,respectively.Results The livability of PC12 cells treated with 100 μmol/L 6-OHDA for 24 h was lower than that of the control group(P0.01).Compared with the 6-OHDA group,GBE at concentrations of 20 and 40 μg/ml could markedly relieve the toxicity of 6-OHDA on PC12 cells,which suggested that GBE could increase the cellular activity and decrease the percentage of cellular apoptosis.The Bax expression was up-regulated in 6-OHDA groups and Bcl-2 expression was down-regulated(P0.05),compared with the control group.Compared with the 6-OHDA group,the Bax expression was down-regulated and Bcl-2 expression was up-regulated in GBE groups,in a dose-dependent manner(P0.05).The difference had statistic significance.Conclusions As one of the causal mechanisms,GBE has inhibitory effects on the apoptosis of the 6-OHDA-induced PC12 cells by up-regulating Bcl-2 expression and down-regulating Bax expression.
Key concepts: Hydroxydopamine, Ginkgo biloba, Apoptosis, Pharmacology, Viability assay, Chemistry, MTT assay, In vitro