Neurochemical effects of the R form of α-lipoic acid and its neuroprotective mechanism in cellular models of Parkinson's disease. (June 2017)

• Record Type: Journal Article
• Authors: Zhao, Hong; Zhao, Xingcheng; Liu, Lijuan; Zhang, Hongxu; Xuan, Mingwen; Guo, Zhaohui; Wang, Hongcai; Liu, Chang
• Is Part Of: International journal of biochemistry & cell biology. Volume 87(2017)
• Page Start: 86
• Page End: 94
• Publication Date: 2017-06
• Subjects: Parkinson's disease -- R form α-lipoic acid -- SH-SY5Y cells -- Neurotoxin -- Neuroprotection; Biochemistry -- Periodicals; Cytology -- Periodicals; Biochemistry -- Periodicals; Cell Biology -- Periodicals; Biochimie -- Périodiques; Cytologie -- Périodiques; Biochimie; Cytologie; Biochemistry; Cytology; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); Periodicals; 572.05
• DOI: 10.1016/j.biocel.2017.04.002
• Languages: English
• ISSNs: 1357-2725

Abstract

Abstract: Objective: Parkinson's disease (PD) is a common neurodegenerative disease. This study aimed to investigate the effects of the R form of α-lipoic acid (RLA) in cellular models of PD induced by 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). Methods: Cell viability and apoptosis were detected using CCK8 and Annexin V-FITC assays, respectively. Intracellular reactive oxygen species (ROS) were detected by fluorescence staining. ELISA assays were performed to detect the levels of dopamine and α-synuclein. To evaluate the effects of RLA on mitochondrial function, cytotoxicity, ATP levels, and mitochondrial gene expression were assayed. Additionally, the expression levels of autophagy-related proteins, including Parkin, PINK1, p62, ATG12, and LC3, were analyzed by western blot, and cell autophagy was visualized by immunofluorescence. Results: RLA increased cell viability and decreased apoptosis, intracellular ROS, and cytotoxicity, and induced cell autophagy in PD models induced by 6-OHDA and MPTP. RLA also reversed the decreased dopamine and increased α-synuclein expression induced by 6-OHDA and MPTP. The mitochondrial regulatory protein PGC-1α was significantly up-regulated by RLA. The expression levels of autophagy-related proteins, including Parkin, PINK1, p62, and ATG12, were down-regulated after RLA treatment, while LC3 expression was up-regulated. Conclusions: RLA has a protective effect against cellular damage induced by 6-OHDA and MPTP. The neuroprotective mechanism of RLA may be associated with improvement of mitochondrial function and autophagy. Therefore, RLA may serve as a promising potential adjuvant for PD treatment.