Sarsasapogenin

416.64

Ethanol：5 mg/mL (12.0 mM)

powder

Sarsasapogenin induces an increase in the population of Hela cells in S phase and an obvious accumulation of cells in G2/M phase in a time-dependent manner. It induces apoptosis in HeLa cells via the caspase-dependent mitochondrial apoptotic pathway. Sarsasapogenin induces the activation of ER stress pathway. Sarsasapogenin induces cytotoxic effects in human cervical cancer cells via cell cycle arrest, ROS-mediated mitochondrial pathway and ER stress pathway. Sarsasapogenin induces the activation of UPR, the ER specific stress response at early stage and then activates CHOP, which may contribute to the initiation and augment of mitochondrial membrane permeabilization by dephosphorylation of Akt so as to mediate the apoptotic signals from ER to mitochondria. Sarsasapogenin potently inhibits NF-κB and MAPK activation, as well as IRAK1, TAK1, and IκBα phosphorylation in LPS-stimulated macrophages. Sarsasapogenin inhibits the binding of LPS to macrophage Toll-like receptor 4, as well as polarization of M2 to M1 macrophages.

Oral administration of sarsasapogenin inhibits 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-κB activation and interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 levels, while simultaneously increasing IL-10. It inhibits Th17 cell differentiation in colonic lamina propria, but induces Treg cell differentiation. Sarsasapogenin potently inhibits inflammatory responses in vivo.

Parigenin; Sarsagenin

C₂₇H₄₄O₃

126-19-2