Gypenoside Attenuates b Amyloid Induced Inflammation in N9 Microglial Cells via SOCS1 Signaling
Reducing b amyloid (Ab induced microglial activation is believed to be effective in treating Alzheimer's disease (AD) Microglia can be activated into classic activated state (M1 state) or alternative activated state (M2 state) and the former is harmful; in contrast, the latter is beneficial. Gypenoside (GP) is the major bioactive constituent of Gynostemma pentaphyllum, a traditional Chinese herb medicine. In this study, we hypothesized that GP attenuates Ab induced microglial activation by ameliorating microglial M1/M2 states, and the process may be mediated by suppressor of cell signaling protein 1 (SOCS1) In this study, we found that Ab exposure increased the levels of microglial M1 markers, including iNOS expression, tumor necrosis factor a (TNF a) interleukin 1b (IL 1b) and IL 6 releases, and coadministration of GP reversed the increase of M1 markers and enhanced the levels of M2 markers, including arginase 1 (Arg 1) expression, IL 10, brain derived neurotrophic factor (BDNF) and glial cell derived neurotrophic factor (GDNF) releases in the Ab treated microglial cells. SOCS1 siRNA, however, significantly abolished the GP induced effects on the levels of microglial M1 and M2 markers. These findings indicated that GP attenuates Ab induced microglial activation by ameliorating M1/M2 states, and the process may be mediated by SOCS1.
Neural plasticity