The Influence Of DSS To Avtivated Microglia Cells And Neuroinflammation Via TLRs/-κB Pathway

Objective:Alzheimer’s disease is a neurodegenerative disease,microglia cells play a pivotal role in the development of AD.Once microglia cells are activated,they release proinflammatory factors that lead to neuroinflammation and neuronal degeneration.Some studies showed that DSS enhanced the memory ability and neuroprotective effects.The aim of this study was to investigate the mechanism of action of DSS in vitro using lipopolysaccharide（LPS）/Aβ₄₂-stimulated BV-2microglia cells.Methods:BV-2 cells were pretreated with 0.58-1.16 mg/mL of DSS for 2 h and then treated with 1μg/mL LPS for 24 h.Cell viability was determined by an 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT）assay.The protein expression levels were measured by Western blots.Inflammatory factors were detected by enzyme-linked immunosorbent assays（ELISAs）.The mRNA levels of inflammatory factors were analyzed by quantitative real-time PCR（qRT-PCR）.And the study of oligomeric Aβ₄₂-inducedBV-2microgliacells also demonstratedthat DSS protect BV-2 microglia cells through the TLRs/NF-κB signaling pathway.Results:DSS treatment at concentrations of 0.58-1.16 mg/mL resulted in no significant cytotoxicity.DSS attenuated the release of pro-inflammatory factors,such as interleukin-1β（IL-1β）,iNOS and tumor necrosis factor-α（TNF-α）in LPS-induced BV-2 cells.DSS attenuated the mRNA expression of pro-inflammatory cytokines,TLR2,and TLR4 and decreased TLR4 and TLR protein levels as well as the phosphorylation of IκB in LPS-induced BV-2 cells.DSS also down-regulated the nuclear translocation of p65.Conclusion:This study demonstrated that DSS has a protective effect on neuroinflammation in LPS/Aβ₄₂-induced BV-2 microglia cells through the TLRs/NF-κB signaling pathway.