Baicalein prevents 6-hydroxydopamine-induced mitochondrial dysfunction in SH-SY5Y cells via inhibition of mitochondrial oxidation and up-regulation of DJ-1 protein expression

• Published in: Molecules (Basel, Switzerland) Vol. 18; no. 12; pp. 14726 - 14738
• Main Authors: Wang, Yue-Hua, Yu, Hai-Tao, Pu, Xiao-Ping, Du, Guan-Hua
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 27.11.2013; MDPI
• Subjects: 6-hydroxydopamine; Aging; Animals; baicalein; Brain - drug effects; Brain - metabolism; brain mitochondria; Cell Line, Tumor; Cell Survival - drug effects; Cells; Disease; Dopamine; Dose-Response Relationship, Drug; Flavanones - chemistry; Flavanones - pharmacology; Humans; Intracellular Signaling Peptides and Proteins - metabolism; Lipid Peroxidation - drug effects; Male; Membrane Potential, Mitochondrial - drug effects; Mitochondria - drug effects; Mitochondria - metabolism; Morphology; Neurodegeneration; Neuropathology; Oncogene Proteins - metabolism; Oxidation; Oxidation-Reduction - drug effects; Oxidative stress; Oxidopamine - pharmacology; Parkinson's disease; Pathogenesis; Phosphorylation; Protein Deglycase DJ-1; Protein expression; Proteins; Rats; Reactive Oxygen Species - metabolism; SH-SY5Y cells; Toxicity; Up-Regulation - drug effects; Beijing China; China
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules181214726

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.