Curcumin

Curcumin is a natural phenolic compound with impressive antioxidant properties. Curcumin is recently proved to exert its chemopreventive effects partly through the activation of nuclear factor (erythroid-2 related) factor 2 (Nrf2) . (In Vitro) :Curcumin exerts its chemopreventive effects partly through the activation of nuclear factor (erythroid-2 related) factor 2 (Nrf2) and its antioxidant and phase II detoxifying enzymes. Curcumin inhibits T47D cells growth, with IC50s of 25, 19 and 17.5 μM for 24, 48 and 72 h MTT assays respectively. IC50s of curcumin and silibinin mixture against T47D cells, are 17.5, 15, and 12 μM for 24, 48, and 72 h exposure times, respectively. Curcumin (2.5-80 μM) induces apoptotic cell death in AGS and HT-29 cell lines, and the IC50 is 21.9±0.1, 40.7±0.5 μM, respectively, in both AGS and HT-29 cell lines. Curcumin-induced apoptosis requires caspase activities in AGS and HT-29 cells. Curcumin induces ER Ca2+ decline and mitochondrial Ca2+ overloading. Curcumin induces the G2/M cell cycle arrest of LNCaP and PC-3 cells in a dose dependent manner. Curcumin upregulates the protein level of NF-kappaB inhibitor IkappaBalpha and downregulates protein levels of c-Jun and AR. (In Vivo) :Curcumin (10 mg/kg, p.o.) significantly prevents decrease in the percentage of sucrose consumption, as compared to the CMS-exposed rats. Curcumin treatment results in significant prevention of increase in TNF-α and IL-6 levels in stressed rats. Curcumin decreases binding of p300/CREB-binding protein (CBP) at the brain-derived neurotrophic factor (BDNF) promoter at 20 mg/kg (i.p.), reduces binding of P300/CBP at the BDNF promoter at 40 mg/kg, and decreases binding all the four proteins of p300/CBP and H3K9ac/H4K5ac at the BDNF promoter at 60 mg/kg in chronic constriction injury (CCI) rats.