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Parkinsons disease (PD) is an age-related neurodegenerative disorder in which the role of Oxidative Stress (OS) is strongly implicated.Pseudoginsenoside-F11 (PF11), a triterpenoid saponins existed from Panax quinquefolium L, has been shown to have antioxidant, anti-ischemic properties and improvement of the function of learning and memory.However, little is known about the effect of PF 11 on the development of Parkinsons disease.The aim of the present study was to investigate the neuroprotective effects of Pseudoginsenoside-F11 (PF 11) on 6-hydroxydopamine (6-OHDA)-induced PD in rats, and explore its potential mechanism.Male Sprague-Dawley (SD) rats were pretreated with PF11 (3, 6, 12 mg/kg, i.g.) once daily for 14 days and unilaterally injected with 6-OHDA (20 μg in 0.1% ascorbic acid in normal saline) into medial forebrain bundle (MFB).After one week of lesioning, rotarod, narrow beam test and rotations were used to study the neuroprotective effect of PF 11.The levels of dopamine (DA) and hydroxy radical (OH) were measured by using high performance liquid chromatography (HPLC) with electrochemical detection to explore the possible mechanism.In the rotarod test, the motor coordination skill was decreased in 6-OHDA-lesioned group rats and was protected significantly by the pretreatment with PF 11.Narrow beam test showed that the mean time taken to cross a 105cm beam was more in 6-OHDA induced lesion rats, but was decreased in the PF11 pretreated group.The present study also showed that PF11 significantly decreased the apomorphine-induced turns in rats and attenuated damage of substantia nigra dopaminergic neurons induced by 6-OHDA in rats.PF11 was found to be successful in preventing 6-OHDA-induced depletion of striatal DA.Conversely, the elevated level of hydroxy radical (OH) induced by 6-OHDA was attenuated significantly in PF11 pretreated group rats.This study indicates that PF11 exerts neuroprotective effect on 6-OHDA-induced Parkinsons disease rat model, and this protection is related to the reduced Oxidative Stress.