Abstract: OBJECTIVE To explore the therapeutic effect and related mechanism of oral administration of FSD-C10 on Parkinson's disease(PD) mice. METHODS Mice were randomly divided into normal group, PD group and FSD-C10 group (50 mg·kg^-1). The total distance, rest time and crossing numbers were evaluated by open field test. Tyrosine hydroxylase(TH) and ROCKⅡ in the brain were detected by Western blotting. Catalase(CAT), glutathione(GSH), malondialdehyde and nitric oxide(NO) were detected by colorimetric method. The levels of inflammatory factors tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6) in the brain were measured by ELISA. RESULTS Compared with the normal group, the total distance and the crossing numbers were decreased(P<0.01), the rest time was increased(P<0.01), the level of TH was decreased(P<0.05), the level of ROCKⅡ was increased(P<0.05), the activity of CAT was decreased(P<0.05), the concentration of GSH was decreased(P<0.01), the concentration of malondialdehyde was increased (P<0.05), and the concentrations of inflammatory factors TNF-α, IL-1β, IL-6 and NO were increased(P<0.05 or P<0.01) in the PD group. Compared with the PD group, the total distance and the crossing numbers were increased(P<0.05), the rest time was decreased(P<0.01), the level of TH was increased(P<0.05), the level of ROCKⅡ was decreased(P<0.05), the activity of CAT was increased(P<0.01), the concentration of GSH was increased(P<0.01), the concentration of malondialdehyde was decreased (P<0.01), and the concentrations of inflammatory factors TNF-α, IL-1β, IL-6 and NO were decreased(P<0.01) in the FSD-C10 group. CONCLUSION Oral administration of FSD-C10 can improve the behavior of PD mice, and has a clear therapeutic effect in PD mice. The therapeutic effect may be related to the recovery of the balance of oxidation-antioxidation system and the reduction of the secretion of inflammatory factors.