Next Article in Journal
Examination of the Potential for Adaptive Chirality of the Nitrogen Chiral Center in Aza-Aspartame
Previous Article in Journal
Design and Synthesis of Arylthiophene-2-Carbaldehydes via Suzuki-Miyaura Reactions and Their Biological Evaluation
Molecules 2013, 18(12), 14726-14738; doi:10.3390/molecules181214726
Article

Baicalein Prevents 6-Hydroxydopamine-Induced Mitochondrial Dysfunction in SH-SY5Y Cells via Inhibition of Mitochondrial Oxidation and Up-Regulation of DJ-1 Protein Expression

1,2,3,* , 4, 1,*  and 2,3,*
1 Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University; Beijing 100191, China 2 Beijing Key Laboratory of Drug Target Identification, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China 3 State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China 4 Jiangsu Kanon Pharmaceutical Co., Ltd, Lianyungang 222047, China
* Authors to whom correspondence should be addressed.
Received: 24 September 2013 / Revised: 18 November 2013 / Accepted: 19 November 2013 / Published: 27 November 2013
Download PDF [809 KB, uploaded 18 June 2014]

Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction is involved in the mechanism of cell damage in Parkinson’s disease (PD). 6-Hydroxydopamine (6-OHDA) is a dopamine analog which specifically damages dopaminergic neurons. Baicalein has been previously reported to have potential in the treatment of PD. The purpose of the present study was to investigate the mechanism of action of baicalein against 6-OHDA injury in SH-SY5Y cells. The results showed that baicalein significantly alleviated alterations of mitochondrial redox activity and mitochondrial membrane potential induced by 6-OHDA in a dose-dependent manner in SH-SY5Y cells compared with vehicle group. Futhermore, baicalein decreased the production of ROS and upregulated the DJ-1 protein expression in SH-SY5Y cells. In addition, baicalein also inhibited ROS production and lipid peroxidation (IC50 = 6.32 ± 0.03 μM) in rat brain mitochondia. In summary, the underlying mechanisms of baicalein against 6-OHDA-induced mitochondrial dysfunction may involve inhibition of mitochondrial oxidation and upregulation of DJ-1 protein expression.
Keywords: baicalein; Parkinson’s disease; 6-hydroxydopamine; SH-SY5Y cells; brain mitochondria baicalein; Parkinson’s disease; 6-hydroxydopamine; SH-SY5Y cells; brain mitochondria
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.

Share & Cite This Article

Further Mendeley | CiteULike
Export to BibTeX |
EndNote
MDPI and ACS Style

Wang, Y.-H.; Yu, H.-T.; Pu, X.-P.; Du, G.-H. Baicalein Prevents 6-Hydroxydopamine-Induced Mitochondrial Dysfunction in SH-SY5Y Cells via Inhibition of Mitochondrial Oxidation and Up-Regulation of DJ-1 Protein Expression. Molecules 2013, 18, 14726-14738.

View more citation formats

Related Articles

Article Metrics

For more information on the journal, click here

Comments

Cited By

[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert