Guoxiang Shen

TL;DR: In vivo and in vitro data generated from the laboratory suggest that many dietary compounds can differentially regulate Nrf2-mediated antioxidant/anti-inflammatory signaling pathways as the first line defense or induce apoptosis once the cells have been damaged.

TL;DR: The results show for the first time that Nrf2(-/-) mice are more susceptible to skin tumorigenesis and that the chemopreventive effects of sulforaphane are mediated, at least in part, through NRF2.

TL;DR: The inhibition of SFN and PEITC on NF-κB transcriptional activation as well as NF-σκB-regulated VEGF, cyclin D1, and Bcl-XL gene expression is mainly mediated through the inhibition of IKK phosphorylation, particularly IKKβ, and the inhibited of IκBα phosphorylated and degradation, aswell as the decrease of nuclear translocation of p65 in PC-3 cells.

TL;DR: Results strongly suggest a model in which PEITC treatment of PC-3 cells activates ERK and JNK, which, in turn, phosphorylate Nrf2 and induce its translocation to the nucleus.

TL;DR: The results showed that ARE activation and Nrf2 protein accumulation were well correlated with phase II gene expression induction, and the structure-activity relationship study indicated that the third sulfur in the structure of OSCs contributed substantially to their bioactivities, and that allyl-containing O SCs were more potent than propyl- containing OSCS.