Sophora flavescens Aiton Decreases MPP + -Induced Mitochondrial Dysfunction in SH-SY5Y Cells

• Published in: Frontiers in aging neuroscience 2018-04, Vol.10, p.119-119
• Main Authors: Kim, Hee-Young, Jeon, Hyongjun, Kim, Hyungwoo, Koo, Sungtae, Kim, Seungtae
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Antibodies; Apoptosis; Bcl-2 protein; Caspase-3; Cytochrome c; Cytotoxicity; DNA fragmentation; DNA nucleotidylexotransferase; Flavonoids; Inflammation; Ischemia; Kinases; Lasers; Membrane potential; Mitochondria; mitochondrial dysfunction; Movement disorders; MPP; Neuroblastoma; Neuroblastoma cells; Neurodegenerative diseases; Neuroscience; PARK7 protein; Parkin protein; Parkinson's disease; Perchloric acid; Proteins; PTEN protein; PTEN-induced putative kinase; SH-SY5Y; Sophora flavescens; Sophora flavescens Aiton; Tetramethylrhodamine methyl ester; Variance analysis
• ISSN: 1663-4365; 1663-4365
• DOI: 10.3389/fnagi.2018.00119

Aiton (SF) has been used to treat various diseases including fever and inflammation in China, South Korea and Japan. Several recent reports have shown that SF has anti-inflammatory and anti-apoptotic effects, indicating that it is a promising candidate for treatment of Parkinson's disease (PD). We evaluated the protective effect of SF against neurotoxin 1-methyl-4-phenylpyridinium ion (MPP )-induced mitochondrial dysfunction in SH-SY5Y human neuroblastoma cells, an PD model. SH-SY5Y cells were incubated with SF for 24 h, after which they were treated with MPP . MPP -induced cytotoxicity and apoptosis were confirmed by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling assay. MitoSOX red mitochondrial superoxide indicator, tetramethylrhodamine methyl ester perchlorate and Parkin, PTEN-induced putative kinase 1 (PINK1), and DJ-1 immunofluorescent staining were conducted to confirm the mitochondrial function. In addition, western blot was performed to evaluate apoptosis factors (Bcl-2, Bax, caspase-3 and cytochrome c) and mitochondrial function-related factors (Parkin, PINK1 and DJ-1). SF suppressed MPP -induced cytotoxicity, apoptosis and collapse of mitochondrial membrane potential by inhibiting the increase of reactive oxidative species (ROS) and DNA fragmentation, and controlling Bcl-2, Bax, caspase-3 and cytochrome expression. Moreover, it attenuated Parkin, PINK1 and DJ-1 expression from MPP -induced decrease. SF effectively suppressed MPP -induced cytotoxicity, apoptosis and mitochondrial dysfunction by regulating generation of ROS, disruption of mitochondrial membrane potential, mitochondria-dependent apoptosis and loss or mutation of mitochondria-related PD markers including Parkin, PINK1 and DJ-1.