Effect of phytoestrogen isoflavone on MPP+-induced apoptosis in PC12 cells

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.