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Lychee Seed Fraction Inhibits Aβ(1-42)-Induced Neuroinflammation in BV-2 Cells via NF-κB Signaling Pathway.

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.

SUBMITTER: Zhao Y

PROVIDER: S-EPMC5925968 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Axonal degeneration is a common pathological feature in many acute and chronic neurological diseases such as spinal cord injury (SCI). SARM1 (sterile alpha and TIR motif-containing 1), the fifth TLR (Toll-like receptor) adaptor, has diverse functions in the immune and nervous systems, and recently has been identified as a key mediator of Wallerian degeneration (WD). However, the detailed functions of SARM1 after SCI still remain unclear. Methods: Modified Allen's method was used to establish a contusion model of SCI in mice. Furthermore, to address the function of SARM1 after SCI, conditional knockout (CKO) mice in the central nervous system (CNS), SARM1Nestin-CKO mice, and SARM1GFAP-CKO mice were successfully generated by Nestin-Cre and GFAP-Cre transgenic mice crossed with SARM1flox/flox mice, respectively. Immunostaining, Hematoxylin-Eosin (HE) staining, Nissl staining and behavioral test assays such as footprint and Basso Mouse Scale (BMS) scoring were used to examine the roles of SARM1 pathway in SCI based on these conditional knockout mice. Drugs such as FK866, an inhibitor of SARM1, and apoptozole, an inhibitor of heat shock protein 70 (HSP70), were used to further explore the molecular mechanism of SARM1 in neural regeneration after SCI. Results: We found that SARM1 was upregulated in neurons and astrocytes at early stage after SCI. SARM1Nestin-CKO and SARM1GFAP-CKO mice displayed normal development of the spinal cords and motor function. Interestingly, conditional deletion of SARM1 in neurons and astrocytes promoted the functional recovery of behavior performance after SCI. Mechanistically, conditional deletion of SARM1 in neurons and astrocytes promoted neuronal regeneration at intermediate phase after SCI, and reduced neuroinflammation at SCI early phase through downregulation of NF-κB signaling after SCI, which may be due to upregulation of HSP70. Finally, FK866, an inhibitor of SARM1, reduced the neuroinflammation and promoted the neuronal regeneration after SCI. Conclusion: Our results indicate that SARM1-mediated prodegenerative pathway and neuroinflammation promotes the pathological progress of SCI and anti-SARM1 therapeutics are viable and promising approaches for preserving neuronal function after SCI.

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Lychee Seed Fraction Inhibits Aβ(1-42)-Induced Neuroinflammation in BV-2 Cells via NF-κB Signaling Pathway.

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