Background: Neuroinflammation is related with the inflammatory stress of brain tissue induced by the activation of microglial in the central nervous system (CNS), which is still an intractable disease for modern clinical system. Chlorogenic acid has multiple biological activities such as antivirus and anti-inflammation, while few researches have revealed its therapeutic functions in neuroinflammation.
Methods: BV2 cells were treated with lipopolysaccharide (LPS) to establish neuroinflammation cell models, and the effects and mechanism of chlorogenic acid in improving the inflammatory progression were investigated. In brief, the toxicity of chlorogenic acid on BV2 cells was detected with MTT assay. The levels of the inflammatory factors including TNF-α, IL-6, IL-1β, and IFN-α were measured with ELISA, and the abundances of TLR4, MyD88, TRIF, and NF-κB were observed by qRT-PCR and western blot.
Results: Chlorogenic acid did not exhibit obvious toxic and side effects on BV2 cells. The levels of TNF-α, IL-6, IL-1β, and IFN-α were observably upregulated in BV2 cells after treating with LPS. Chlorogenic acid significantly reduced the levels of TNF-α, IL-6, IL-1β, and IFN-α. Moreover, the abundances of TLR4, MyD88, TRIF, and NF-κB were increased in LPS-induced BV2 cells, while chlorogenic acid could obviously reduce their expressions.
Conclusion: This study suggests that chlorogenic acid can improve the inflammatory stress of LPS-induced BV2 cell via interacting with the TLR4-mediated downstream pathway, which is a potential drug for neuroinflammation treatment.
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