Cerevisterol is a cytotoxic steroid, can inhibit the activity of DNA polymerase alpha. It can stimulate NGF-mediated neurite outgrowth on PC12 cells. Cerevisterol acts as a natural agent for treating inflammatory diseases by targeting an MAPK, NF-κB, AP-1, and Nrf2-mediated HO-1 signaling cascade.

Cerevisterol suppresses the LPS-induced production of NO and PGE2, which is a plausible mechanism for this effect is by reducing the expression of iNOS and COX-2. Cerevisterol also decreases the expression of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β. Cerevisterol halted the nuclear translocation of NF-κB by blocking the phosphorylation of inhibitory protein κBα (IκBα) and suppressing NF-κB transactivation. The mitogen-activated protein kinases (MAPK) signaling pathways are also suppressed. Cerevisterol treatment also inhibited the transactivation of AP-1 and the phosphorylation of c-Fos. Furthermore, Cerevisterol could induce the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) by down-regulating Kelch-like ECH-associated protein 1 (Keap-1) and up-regulating hemeoxygenases-1 (HO-1) expression.