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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 182495, 8 pages
Research Article

The Impact of Paeoniflorin on α-Synuclein Degradation Pathway

1Lianyungang First People’s Hospital Postdoctoral Innovative Practice Base, Nanjing Medical University Postdoctoral Research Station, Lianyungang 222002, China
2Department of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China
3Department of Emergency, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China

Received 11 August 2015; Revised 8 November 2015; Accepted 11 November 2015

Academic Editor: Giuseppe Esposito

Copyright © 2015 Zenglin Cai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Paeoniflorin (PF) is the major active ingredient in the traditional Chinese medicine Radix. It plays a neuroprotective role by regulating autophagy and the ubiquitin-proteasome degradation pathway. In this study, we found PF significantly reduced cell damage caused by MPP+, returning cells to normal state. Cell viability significantly improved after 24 h exposure to RAPA and PF in the MPP+ group (all ). CAT and SOD activities were significantly decreased after PF and RAPA treatment, compared with MPP+ (). In addition, MPP+ activated both LC3-II and E1; RAPA increased LC3-II but inhibited E1. PF significantly upregulated both LC3-II (autophagy) and E1 (ubiquitin-proteasome pathway) expression (), promoted degradation of α-synuclein, and reduced cell damage. We show MPP+ enhanced immunofluorescence signal of intracellular α-synuclein and LC3. Fluorescence intensity of α-synuclein decreased after PF treatment. In conclusion, these data show PF reversed the decline of proteasome activity caused by MPP+ and significantly upregulated both autophagy and ubiquitin-proteasome pathways, promoted the degradation of α-synuclein, and reduced cell damage. These findings suggest PF is a potential therapeutic medicine for neurodegenerative diseases.