摘要
Objectives： Chunghyuldan （CHD）, a combinatorial drug that has anti-hyperlipidemic and anti inflammatory activities, has been shown to reduce infarct volume in a focal ischemia-reperfusion rat model. To explore the molecular basis of CHD＇s neuroprotective effect, we examined whether CHD shows a cell-protective activity and has a regulatory effect on Bax and/or B-cell leukemia/lymphoma 2 （Bcl-2） expression in mouse neuroblastoma 2a （N2a） cells subjected to hypoxia-reoxygenation （H/R）. Methods： In order to evaluate the effects of CHD on the cytotoxicity induced from hypoxia or H/R condition, lactate dehydrogenase （LDH） assay was performed. To explore whether the suppression of neural damage when pre-treated with CHD is associated with its anti-apoptotic effect, the CHD effect on the expression of Bcl-2 and Bax was analyzed by Western blotting analysis. Results： Cytotoxicity of N2a cell line was slightly increased in 42 h hypoxia condition and dramatically increased under the H/R condition. CHD treatment markedly decreased the cytotoxicity in both conditions （P〈0.01, P〈0.05）. H/R markedly increased the expression of the pro-apoptotic protein, Bax, but slightly increased the expression of the anti-apoptotic protein, Bcl-2, compared with the normoxia or hypoxia group. CHD significantly decreased Bax expression （P〈0.01） and slightly decreased Bcl-2 expression （P〉0.05）, resulted in a reduction of Bax/Bcl-2 ratio in N2a cells subjected to H/R. Conclusion： CHD has neuroprotective effect in N2a cells subjected to H/R, which might be derived at least in part from its ability to decrease the expression of the pro-apoptotic protein, Bax.
Objectives： Chunghyuldan （CHD）, a combinatorial drug that has anti-hyperlipidemic and anti inflammatory activities, has been shown to reduce infarct volume in a focal ischemia-reperfusion rat model. To explore the molecular basis of CHD＇s neuroprotective effect, we examined whether CHD shows a cell-protective activity and has a regulatory effect on Bax and/or B-cell leukemia/lymphoma 2 （Bcl-2） expression in mouse neuroblastoma 2a （N2a） cells subjected to hypoxia-reoxygenation （H/R）. Methods： In order to evaluate the effects of CHD on the cytotoxicity induced from hypoxia or H/R condition, lactate dehydrogenase （LDH） assay was performed. To explore whether the suppression of neural damage when pre-treated with CHD is associated with its anti-apoptotic effect, the CHD effect on the expression of Bcl-2 and Bax was analyzed by Western blotting analysis. Results： Cytotoxicity of N2a cell line was slightly increased in 42 h hypoxia condition and dramatically increased under the H/R condition. CHD treatment markedly decreased the cytotoxicity in both conditions （P〈0.01, P〈0.05）. H/R markedly increased the expression of the pro-apoptotic protein, Bax, but slightly increased the expression of the anti-apoptotic protein, Bcl-2, compared with the normoxia or hypoxia group. CHD significantly decreased Bax expression （P〈0.01） and slightly decreased Bcl-2 expression （P〉0.05）, resulted in a reduction of Bax/Bcl-2 ratio in N2a cells subjected to H/R. Conclusion： CHD has neuroprotective effect in N2a cells subjected to H/R, which might be derived at least in part from its ability to decrease the expression of the pro-apoptotic protein, Bax.
