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PPAR Research
Volume 2017, Article ID 4089214, 12 pages
Research Article

Neuroprotective Effect and Mechanism of Thiazolidinedione on Dopaminergic Neurons In Vivo and In Vitro in Parkinson’s Disease

1Department of Physiology, College of Life Science, Hebei Normal University, Shijiazhuang, Hebei 050024, China
2Human Movement Science, Hebei Institute of Physical Education, Shijiazhuang, Hebei 050041, China
3Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, China

Correspondence should be addressed to Zhenlong Guan; nc.ude.utbeh.liam@06nauglz

Received 29 August 2016; Revised 8 December 2016; Accepted 21 December 2016; Published 5 March 2017

Academic Editor: Maria Paola Cerù

Copyright © 2017 Yanqin Wang 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.


The aim of the present study was to gain insight into the neuroprotection effects and mechanism of thiazolidinedione pioglitazone in both in vitro and in vivo MPP+/MPTP induced PD models. In vivo experimental results showed that oral treatment of pioglitazone resulted in significant improvements in behavior symptoms damaged by MPTP and increase in the survival of TH positive neurons in the pioglitazone intervention groups. In addition, oral treatment of pioglitazone increased the expression of peroxisome proliferator-activated receptor-γ coactivator of 1 (PGC-1) and increased the number of mitochondria, along with an observed improvement in mitochondrial ultrastructure. From in vitro studies, 2,4-thiazolidinedione resulted in increased levels of molecules regulated function of mitochondria, including PGC-1, nuclear respiratory factor 1 (NRF1), NRF2, and mitochondria fusion 2 (Mfn2), and inhibited mitochondria fission 1 (Fis1). We show that protein levels of Bcl-2 and ERK were reduced in the MPP+-treated group compared with the control group. This effect was observed to be reversed upon treatment with 2,4-thiazolidinedione, as Bcl-2 and ERK expression levels were increased. We also observed that levels of the apoptotic protein Bax showed opposite changes compared to Bcl-2 and ERK levels. The results from this study confirm that pioglitazone/2,4-thiazolidinedione is able to activate PGC-1 and prevent damage of dopaminergic neurons and restore mitochondria ultrastructure through the regulation of mitochondria function.