Benzyl sulforaphane is superior to sulforaphane in inhibiting the Akt/MAPK and activating the Nrf2/ARE signalling pathways in HepG2 cells

Objectives Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, has been reported to own anticarcinogenic, antiinflammatory and cancer chemopreventive properties. Benzyl sulforaphane (BSFN) was a derivative of SFN which was designed and synthesized by our laboratory. Here, the cancer prevention and anticancer effects of BSFN on human hepatoma (HepG2) cells were investigated. Methods Key findings The following effects of BSFN on components of the mitochondrial apoptotic pathway were examined: generation of reactive oxygen species and mitochondrial membrane potential (Delta psi m) changes by flow cytometry, the expression changes of Bcl-2 family proteins and Akt/MAPK proteins by western blot. The protein levels of Nrf2 and Keap1 were also tested via Western blot. The effects of BSFN on Nrf2 nuclear translocation and ARE-reporter gene activity were examined by fluorescence microscope and multifunctional spectrophotometer. Benzyl sulforaphane could induce cell apoptosis by mitochondrion-dependent pathway, which inhibited HepG2 cells growth in a manner of time- and concentration -dependent. Furthermore, BSFN could inhibit the Akt/MAPK and activate the Nrf2/ARE pathway in HepG2 cells. Conclusions Benzyl sulforaphane was superior to SFN in inhibiting Akt/MAPK and activating Nrf2/ARE signalling pathways in HepG2 cells, which indicated that BSFN could be a safe therapeutic strategy for the prevention and treatment of liver cancer.