Hordenine inhibits neuroinflammation and exerts neuroprotective effects via inhibiting NF-κB and MAPK signaling pathways in vivo and in vitro
Abstract
Parkinson's disease (PD) is a usual disease caused by degeneration of the central nervous system, which features the denaturation and death of dopaminergic neurons in the substantia nigra compact (SNc) of the midbrain. Neuroinflammation casts a consequential role in its pathogenesis, and the excessive activation of microglia as a major part of neuroinflammation cannot be ignored. Studies have indicated that Hordenine (HOR) functioned widely as an anti-oxidant and anti-inflammatory substance, but there are no reports on neuroinflammation effects. Therefore, this study is devoted to exploring the effect of HOR on neuroinflammation and its specific mechanism. In vivo, results revealed that HOR depressed the activation of microglia in SNc and protected dopaminergic neurons in the 6-hydroxydopamine (6-OHDA)-induced PD rat model, which terminally reduced movement disorders and weight loss. In vitro, studies have shown that HOR can inhibit inflammatory responses triggered by lipopolysaccharide (LPS) in BV-2 cells. More profound studies have discovered that the specific anti-inflammatory mechanism is intimately associated with the NF-κB and MAPK signaling pathways. All in it together, HOR acts as a significant role in preserving dopaminergic neurons by restraining neuroinflammation mediated by activation of microglia. This may provide a potential drug for Parkinson's treatment.
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Hordenine inhibits loss of dopaminergic neurons in a Parkinson's disease rat model.
“They found, through immunohistochemistry and Western blotting, that hordenine inhibits the loss of dopaminergic neurons.”
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- Authors
- Su, Y., Liu, Y., He, D., Hu, G., Wang, H., Ye, B., He, Y., Gao, X., & Liu, D.
- Affiliations
- Jilin University (CN)
- The Catholic University of Korea Seoul St. Mary's Hospital (KR)
- Corresponding author
- Liu, Yanting
- Liu, Dianfeng
- Venue
- International Immunopharmacology
- Publisher
- Elsevier BV
- Published
- 2022-07
- Volume
- 108
- Pages
- 108694
- ISSN
- 1567-5769 (ISSN-L)
- OpenAlex
- W4220990437
- Cited by
- 26
- References
- 47
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 3
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- International Immunopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31772547)
- Fundamental Research Funds for the Central Universities
- Jilin Scientific and Technological Development Program (20200703011ZP)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- hordenine, Parkinson's disease, neuroinflammation, neuroprotection, microglial activation, dopaminergic neurons, substantia nigra pars compacta, NF-κB signaling, MAPK signaling, 6-hydroxydopamine, lipopolysaccharide, BV-2 cells, anti-inflammatory agents
- MeSH terms
- Neuroinflammatory Diseases, Animals, Anti-Inflammatory Agents, Cell Line, Lipopolysaccharides, Parkinson Disease, Tyramine, NF-kappa B, Microglia, Neuroprotective Agents, MAP Kinase Signaling System, Rats
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