Previous studies have shown that estrogen may reduce neurological damages in Parkinson's diseasebut the mechanisms of this protective effect are unclear. This study was designed to investigate theeffect of isoflavone, a plant-derived estrogen, on the apoptosis of an in vitro cell model for Parkinson'sdisease. This cell model was based on 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis in PC12cells. PC12 cells were divided into four groups: control (vehicle), MPP+ (250 -- CORRECTION REQUIRED HERE -- 2;mol/L) only, isoflavone(10 -- CORRECTION REQUIRED HERE -- 2;M)+MPP+ (250 -- CORRECTION REQUIRED HERE -- 2;mol/L), and isoflavone (10 -- CORRECTION REQUIRED HERE -- 2;M) only group. Bax protein in PC12 cells was measuredwith Western-blot. The expression of Bax gene was analysed by in situ hybridization assay. The apoptosisratio in the isoflavone +MPP+ group (30.9%) and the control group (30.7%) was similar (P > 0.05), butit was lower than in the MPP+ group (67.9%, P < 0.05). Optical density in the Bax positive cells in theisoflavone +MPP+ group was lower than in the MPP+ group (0.28±0.03 vs 0.45±0.06, P < 0.05). BaxmRNA in the isoflavone +MPP+ group was lower than in the MPP+ group (0.23±0.02 vs 0.47±0.04,P < 0.01). The Bax protein in the isoflavone +MPP+ group was also lower than in the MPP+ group (89±12vs 131±19, P < 0.01). In conclusion, soflavone suppressed MPP+-induced apoptosis in PC12 cells. Theapoptosis suppression is associated with a decreased level of proapoptotic Bax gene and Bax protein.Further studies are warranted to investigate the clinical effect of isoflavone on Parkinson's disease.