Gypenoside Attenuates β Amyloid-Induced Inflammation in N9 Microglial Cells via SOCS1 Signaling

摘要: Reducing β amyloid- (Aβ-) induced microglial activation is believed to be effective in treating Alzheimer's disease (AD). Microglia can activated into classic state (M1 state) or alternative (M2 state), and the former harmful; contrast, latter beneficial. Gypenoside (GP) major bioactive constituent of Gynostemma pentaphyllum, a traditional Chinese herb medicine. In this study, we hypothesized that GP attenuates Aβ-induced by ameliorating M1/M2 states, process may mediated suppressor cell signaling protein 1 (SOCS1). found Aβ exposure increased levels M1 markers, including iNOS expression, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-6 releases, coadministration reversed increase markers enhanced M2 arginase-1 (Arg-1) IL-10, brain-derived neurotrophic (BDNF), glial cell-derived (GDNF) releases Aβ-treated cells. SOCS1-siRNA, however, significantly abolished GP-induced effects on markers. These findings indicated SOCS1.