Baicalin Represses C/EBPβ via Its Antioxidative Effect in Parkinson’s Disease

• Published in: Oxidative medicine and cellular longevity Vol. 2020; no. 2020; pp. 1 - 14
• Main Authors: Jin, Lingjing, Tong, Weifang, Zhang, Jingxing, Zhang, Liwen, He, Yijing, Shen, Yijue, Lei, Kecheng, Xu, Yichun
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2020; Hindawi; Hindawi Limited
• Subjects: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; alpha-Synuclein - metabolism; Animals; Antioxidants - pharmacology; CCAAT-Enhancer-Binding Protein-beta - metabolism; Cell Line; Cytotoxicity; Disease; Dopaminergic Neurons - drug effects; Dopaminergic Neurons - metabolism; Dopaminergic Neurons - pathology; Flavonoids; Flavonoids - chemistry; Flavonoids - pharmacology; Gene expression; Gene Ontology; Humans; Inflammation - pathology; Male; Mice, Inbred C57BL; Mitochondria - drug effects; Mitochondria - metabolism; Molecular Sequence Annotation; Motor Activity - drug effects; Neurodegeneration; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurotoxins - toxicity; Oxidation-Reduction; Oxidative stress; Oxidative Stress - drug effects; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parkinson Disease - physiopathology; Parkinson's disease; Pathology; Phosphorylation; Proteins; United States > US; California
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2020/8951907

Parkinson’s disease (PD) is a neurodegenerative disease characterized by the gradual loss of dopaminergic (DA) neurons in the substantia nigra (SN) and the formation of intracellular Lewy bodies (LB) in the brain, which aggregates α-synuclein (α-Syn) as the main component. The interest of flavonoids as potential neuroprotective agents is increasing due to its high efficiency and low side effects. Baicalin is one of the flavonoid compounds, which is a predominant flavonoid isolated from Scutellaria baicalensis Georgi. However, the key molecular mechanism by which Baicalin can prevent the PD pathogenesis remains unclear. In this study, we used bioinformatic assessment including Gene Ontology (GO) to elucidate the correlation between oxidative stress and PD pathogenesis. RNA-Seq methods were used to examine the global expression profiles of noncoding RNAs and found that C/EBPβ expression was upregulated in PD patients compared with healthy controls. Interestingly, Baicalin could protect DA neurons against reactive oxygen species (ROS) and decreased C/EBPβ and α-synuclein expression in pLVX-Tet3G-α-synuclein SH-SY5Y cells. In a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD mouse model, the results revealed that treatment with Baicalin improved the PD model’s behavioral performance and reduced dopaminergic neuron loss in the substantia nigra, associated with the inactivation of proinflammatory cytokines and oxidative stress. Hence, our study supported that Baicalin repressed C/EBPβ via redox homeostasis, which may be an effective potential treatment for PD.