ArticleFrontiers in pharmacology2018
Lychee Seed Fraction Inhibits Aβ(1-42)-Induced Neuroinflammation in BV-2 Cells via NF-κB Signaling Pathway.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 19 citations in OpenAlex.
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- ADMSC Exo-MicroRNA-22 improve neurological function and neuroinflammation in mice with Alzheimer's disease.Journal of cellular and molecular medicine · 2021Article
- Targeting TDP-43 Pathology Alleviates Cognitive and Motor Deficits Caused by Chronic Cerebral Hypoperfusion.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Design and Synthesis of New Benzo[d]oxazole-Based Derivatives and Their Neuroprotective Effects on β-Amyloid-Induced PC12 Cells.Molecules (Basel, Switzerland) · 2020Article
- Mechanism of microRNA-22 in regulating neuroinflammation in Alzheimer's disease.Brain and behavior · 2020Article
- The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response.Molecules (Basel, Switzerland) · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In our previous studies, an active fraction derived from lychee seed could inhibit β-amyloid-induced apoptosis of PC12 cells and neurons. The primarily microglia cells are recognized as the brain's resident macrophages and thought to remodel of the brain by removing presumably redundant, apoptotic neurons. In the current study, we aimed to investigate the anti-neuroinflammation effect of lychee seed fraction (LSF) in Aβ(1-42)-induced BV-2 cells and the underlying mechanism. The morphology results displayed that LSF could improve the status of Aβ(1-42)-induced BV-2 cells. The enzyme-linked immunosorbent assay, real-time PCR, and Western blotting results showed that LSF could significantly reduce the release, mRNA levels, and protein expressions of the pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in Aβ(1-42)-induced BV-2 cells, which were downregulated through suppressing the NF-κB signaling pathway. Furthermore, LSF could upregulate Bcl-2 and downregulate Bax, Caspase-3, and cleaved-PARP protein expressions. Taken together, our results first demonstrated that LSF could suppress the inflammatory response via inhibiting NF-κB signaling pathway, and inhibit apoptosis in Aβ(1-42)-induced BV-2 cells. Our findings further prove that LSF as a potential drug may be used for treating AD in the future.
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