Objectives:Chunghyuldan(CHD),a combinatorial drug that has anti-hyperlipidemic and antiinflammatory 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 Westem 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-apoptoUc 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 antiinflammatory 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) 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 Westem blotting analysis. Results: Cytotoxicity of N2a cell line was slightly increased in 42 h hypoxia condition and increased increased under the H / R condition. CHD treatment marked l H / R markedly increased the expression of the pro-apoptotic protein, Bax, but slightly increased the expression of the anti-apoptoUc protein, Bcl-2, compared (P <0.01, P < (P> 0.05), resulting in a reduction of Bax / Bcl-2 ratio in N2a cells by H / R. Conclusion: CHD has a 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.