Platycodin D inhibits MPP+-induced inflammatory response in BV-2 cells through the TLR4/MyD88/NF-κB signaling pathway

Parkinson's disease is a common progressive neurodegenerative disorder associated with inflammation. Platycodin D (PLD) is a triterpenesaponin that has anti-inflammatory and neuro-protective effects. However, the role of PLD in Parkinson's disease has not been fully investigated. In the current study, we investigated the effect of PLD on 1-methyl-4-phenylpyridinium (MPP+)-induced inflammatory response in BV-2 cells. Our results showed that PLD treatment improved the cell viability of MPP+-induced BV-2 cells. PLD significantly inhibited the levels of inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in MPP+-treated BV-2 cells. The increased productions of inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6 in MPP+-treated BV-2 cells were also suppressed by PLD. Furthermore, PLD inhibited the activation of TLR4/MyD88/NF-kappa B pathway in MPP+-treated BV-2 cells. Overexpression of TLR4 reversed the protective effects of PLD on MPP+-treated BV-2 cells. Collectively, PLD protected BV-2 cells from MPP+-induced inflammatory response via regulating the TLR4-MyD88-NF-kappa B signaling pathway.