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Parkinson’s Disease
Volume 2015 (2015), Article ID 931058, 11 pages
Research Article

Enhanced Neuroprotective Effects of Coadministration of Tetrandrine with Glutathione in Preclinical Model of Parkinson’s Disease

1Department of Geriatrics Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China
2Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China
3Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China
4Department of Emergency Neurology, The Affiliated Hospital of Medical College Qingdao University, Qingdao 266021, China
5Department of Neurology, Shanghai 9th People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
6Department of Neurology, Suzhou Municipal Hospital Affiliated to Nanjing Medicine University, Suzhou 215001, China

Received 22 July 2015; Revised 13 October 2015; Accepted 20 October 2015

Academic Editor: Francisco Grandas

Copyright © 2015 Xiang-Yun Li 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.


Aim. In this study we examined the influence of tetrandrine (Tet) on the neuroprotective effects of glutathione (GSH) in the 6-hydroxydopamine- (6-OHDA-) lesioned rat model of Parkinson’s disease (PD). Methods. Levels in the redox system, dopamine (DA) metabolism, dopaminergic neuronal survival, and apoptosis of the substantia nigra (SN) and striatum, as well as the rotational behavior of animals were examined after a 50-day administration of GSH + Tet (or GSH) and/or L-3,4-dihydroxyphenylalanine (L-dopa) to PD rats. Ethics Committee of Huashan Hospital, Fudan University approved the protocol (number SYXK2009-0082). Results. Administration of GSH or Tet alone did not show any significant effects on the factors evaluated in the PD rats. However, in the GSH + Tet group, we observed markedly decreased oxidative damage, inhibition of DA metabolism and enhanced DA synthesis, increased tyrosine hydroxylase- (TH-) immunopositive neuronal survival, and delayed apoptosis of dopaminergic neurons in the SN. Animal rotational behavior was improved in the GSH + Tet group. Additionally, coadministration of GSH + Tet appeared to offset the possible oxidative neurotoxicity induced by L-dopa. Conclusion. In this study, we demonstrated that tetrandrine allowed occurrence of the neuroprotective effect of glutathione probably due to inhibition of P-glycoprotein on 6-hydroxydopamine-lesioned rat models of Parkinson’s disease, including rats undergoing long-term L-dopa treatment.