Sulforaphane is derived from the consumption of cruciferous vegetables, such as broccoli. It has shown anticancer and cardioprotective activities.
Sulforaphane induces a cell cycle arrest in a dose-dependent manner, followed by cell death. This sulforaphane-induced cell cycle arrest was correlated with an increased expression of cyclins A and B1. Sulforaphane induces cell death via an apoptotic process. Sulforaphane inhibits the reinitiation of growth and diminishes cellular viability in quiescent colon carcinoma cells (HT29) and has lower toxicity on differentiated CaCo2 cells . Pre-treatment of H9c2 rat myoblasts with sulforaphane decreases the apoptotic cell number and the expression of pro-apoptotic proteins, as well as the doxorubicin-induced increase in mitochondrial membrane potential. Furthermore, sulforaphane increases the mRNA and protein expression of heme oxygenase-1, which consequently reduces the levels of reactive oxygen species in the mitochondria which are induced by doxorubicin .
Administration of sulforaphane reduces the incidence, multiplicity, and weights and delays the development of the mammary tumors evoked by a single dose of DMBA in female SD rats .
HT29 cells are seeded at low density (5×10^4 cells/mL) in 35- or 120-mm diameter Primaria dishes in standard medium containing 5% FCS. One day after seeding, the medium is changed, and HT29 cells are treated with sulforaphane (0-30 μM). An equivalent amount of the solvent (ethanol) is added to control cells (0.2% final concentration). The drug effect on cellular viability is evaluated using the MTT assay .
At age 47, 48, 49, 50, and 51 days, each animal receives by gavage either 0.5 mL of Emulphor EL-620 alone or the specified doses (75, 100, or 150 μM daily) of sulforaphane or compound 2, 3, or 4 in 0.5 mL of Emulphor EL-620. On day 50, 3 hr after administration of the vehicle or protector, all rats also receive an intragastric instillation of 8.0 mg of DMBA dissolved in 1.0 mL of sesame oil. This dose of DMBA is selected to produce a substantial tumor incidence, but not one so high as to overwhelm a potential chemoprotective effect. The animals are examined once weekly for the appearance and location of palpable tumors. At age 202 days, i.e., 152 days after carcinogen administration, all animals are euthanized with ether and weighed. The tumors are separated from the fat and connective tissue by dissection weighed and fixed in buffered 10% formalin. All tumors are identified microscopically by examination of stained sections .