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

Yue-Hua Wang¹  Hai-Tao Yu²  Xiao-Ping Pu¹ 

[1] Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University; Beijing 100191, China;Jiangsu Kanon Pharmaceutical Co., Ltd, Lianyungang 222047, China

关键词: baicalein;    Parkinson’s disease;    6-hydroxydopamine;    SH-SY5Y cells;    brain mitochondria;   

DOI  :  10.3390/molecules181214726

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.