Gypenoside

Gypenoside（Gyp) has an activity of anti-inflammatory, anti-thrombotic, antioxidative and anti-cancer actions. Gypenoside inhibited SW-480 cell proliferation in a dose- and time-dependent manner. Gyp is capable of exerting different alternative cytotoxicity in cancer cells and normal cells, which might be potentially useful as a cancer preventive or treatment agent. Gyp could cause cell membrane integrity damage, decrease the Δψm level, induce DNA fragmentation and initiate apoptotic response in SW-480 cells. ROS generated in SW-480 cells play an important role in Gyp induced cell death. Gyp induces microfilament network collapse and injures the cell shape and migration ability^[1]. It is reported that Gypenoside can induce neuroprotection against Aβ in vitro. Gypenoside attenuates Aβ-induced microglial activation, decreases the levels of microglial M1 state (classic activated state) markers, including iNOS protein expression, TNF-α, IL-1β, and IL-6 releases, and increases the levels of M2 markers, such as Arg-1 protein expression, IL-10, BDNF, and GDNF secretions from the cells. Gypenoside reduces the Aβ-induced microglial activation by shifting microglial M1 to M2 (alternative activated state) state, and the SOCS1 protein may mediate the process^[2].

Gypenoside has been known for its wide beneficial effects for treating hepatitis, hyperlipoproteinemia and cardiovascular disease^[1].

To investigate the effect of Gypenoside on SW-480 cell proliferation, cells are seeded in 96-well plates. Various concentrations (0, 70, 100 and 130 µg/ml; 80% ethanol is used as the solvent control) of Gypenoside are added and the cells are incubated for various periods of time, at a density of 1×10⁵ cells/ml, respectively. The cell viability is determined by using MTT assay. The absorbance at 570 nm is recorded using a microplate reader.

• [1] Yan H, et al. PLoS One. 2014, 9(4):e95609.
• [2] Hui Cai, et al. Neural Plasticity. 2016.