Farrerol attenuates MPP+-induced inflammatory response by TLR4 signaling in a microglia cell line

Farrerol was found to possess neuroprotective effect; however, the mechanism remains unknown. The aim of the present study was to explore the effect of farrerol on MPP+-induced inflammation in mouse microglial BV-2 cells and to elaborate the underlying mechanism. MTT assay was performed to measure the cell viability. The pro-inflammatory mediators and cytokines including interleukin (IL)-6, IL-1, and tumor necrosis factor- (TNF-); inducible nitric oxide synthase; and cyclooxygenase 2 were measured. The expression of p-p65, p-IB, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 were analyzed by western blot. We found that farrerol treatment improved cell viability in MPP+-induced BV-2 cells. MPP+-induced upregulation of IL-6, IL-1, and TNF- was inhibited by farrerol treatment. Farrerol treatment also attenuated MPP+-induced expression of inducible nitric oxide synthase and cyclooxygenase 2 as well as the activation of NF-B in BV-2 cells. MPP+-induced TLR4 signaling was markedly diminished by farrerol treatment. Knockdown of TLR4 attenuated MPP+-induced inflammatory response in BV-2 cells. In conclusion, farrerol treatment attenuated MPP+-induced inflammatory response by inhibiting the TLR4 signaling pathway in BV-2 cells. The results indicated that farrerol could be used as a therapeutic agent for preventing or alleviating the neuroinflammation-related diseases, such as Parkinson's disease.