Sulforaphane

Sulforaphane is an orally active inducer of the Keap1/Nrf2/ARE pathway. Sulforaphane promotes the transcription of tumor-suppressing proteins and effectively inhibits the activity of HDACs. Through the activation of the Keap1/Nrf2/ARE pathway and further induction of HO-1 expression, Sulforaphane protects the heart. Sulforaphane suppresses high glucose-induced pancreatic cancer through AMPK-dependent signal transmission. Sulforaphane exhibits both anticancer and anti-inflammatory properties^{[1][2][3][4][5][6]}. In Vitro:Sulforaphane (0-30 μM) induces cell cycle arrest and apoptosis in a dose-dependent manner. Sulforaphane-induced cell cycle arrest is associated with an increase in the expression of cyclin A and B1^[1].
Sulforaphane (0-30 μM) inhibits the re-initiation of growth and decreases cell viability in HT29 cells, exhibiting lower toxicity towards differentiated cells^[1].
Sulforaphane (10 μM, 24 hours) pre-treatment reduces the number of apoptotic cells, decreases the expression of pro-apoptotic proteins (Bax, caspase-3, cytochrome c), and counteracts the increase in mitochondrial membrane potential induced by Doxorubicin (HY-15142A) (1 μM, 2 hours) in H9c2 cells^[2]. Sulforaphane (10 μM, 2 or 24 hours) effectively reduces ROS production and cell apoptosis in H9c2 cells induced by Doxorubicin (1 μM, 2 or 24 hours) through the activation of the Keap1/Nrf2/ARE pathway and further induction of HO-1 expression^[2]. In Vivo:Sulforaphane (13.3, 17.7, 26.6 mg/kg; Oral gavage; 5 days) is capable of inhibiting the formation of mammary tumors in female Sprague-Dawley rats following a single-dose treatment with DMBA (HY-W011845) (8 mg/mL)^[3].
Sulforaphane (13.3, 17.7, 26.6 mg/kg; Oral gavage; 5 days) can reduce the incidence, multiplicity, and weight of mammary tumors induced by DMBA (8 mg/mL) in female Sprague-Dawley rats, and delay their development^[3].