Baicalin Represses C/EBP β via Its Antioxidative Effect in Parkinson's Disease

• Type of Material: Article
• Authors: Kecheng Lei, Emory University; Yijue Shen, Tongji University School of Medicine; Yijing He, Tongji University School of Medicine; Liwen Zhang, Shanghai Biochip Limited Corporation; Jingxing Zhang, Tongji University School of Medicine; Weifang Tong, Tongji University School of Medicine; Yichun Xu, Emory University; Lingjing Jin, Tongji University School of Medicine
• Language: English
• Date: 2020-01-01
• Publisher: Hindawi
• Publication Version: Final Published Version
• Copyright Statement: © 2020 Kecheng Lei et al.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1155/2020/8951907
• Title of Journal or Parent Work: Oxidative Medicine and Cellular Longevity
• Volume: 2020
• Start Page: 8951907
• End Page: 8951907
• Grant/Funding Information: This article is supported by the “National Key R&D Program of China” (2018YFC1314700 and 2018YFA0108000), National Natural Science Foundation of China (81974196 and 81873779), Shanghai municipal medical and health excellent academic leaders training program (2017BR029), and China Postdoctoral Science Foundation (2018M632168).
• Keywords: Antioxidants; Molecular Sequence Annotation; Humans; Oxidative Stress; alpha-Synuclein; Cell Line; Male; CCAAT-Enhancer-Binding Protein-beta; Animals; Neuroprotective Agents; Neurotoxins; Mice, Inbred C57BL; Flavonoids; Mitochondria; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Motor Activity; Gene Ontology; Oxidation-Reduction; Dopaminergic Neurons; Parkinson Disease; Inflammation
• Research Categories: Biology, Genetics; Biology, Cell; Health Sciences, Pathology; Engineering, Biomedical

Abstract

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.