Curcumin

Curcumin (Diferuloylmethane), a natural phenolic compound, is a p300/CREB-binding protein-specific inhibitor of acetyltransferase, represses the acetylation of histone/nonhistone proteins and histone acetyltransferase-dependent chromatin transcription. Curcumin is a photosensitizer against microorganisms. Curcumin shows inhibitory effects on NF-κB and MAPKs, and has diverse pharmacologic effects including anti-inflammatory, antioxidant, antiproliferative and antiangiogenic activities. Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. IC50 & Target:Keap1-Nrf2^[1], Histone acetyltransferase^[6] 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^[1].
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 (HY-N0779A) mixture against T47D cells, are 17.5, 15, and 12 μM for 24, 48, and 72 h exposure times, respectively^[2].
Curcumin (2.5-80 μM) induces apoptotic cell death in AGS and HT-29 cell lines, and the IC₅₀ values are 21.9, 40.7 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^[3].
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^[5].
Curcumin (0 μM, 4 μM and 8 μM; for 24 h) can significantly inhibit the decrease in Bcl-2 gene expression caused by H2O2 and can significantly inhibit the increase in Bax and Caspase-3 gene expression induced by H₂O₂. Curcumin can alleviate apoptosis in bovine adipose-derived stem cells (ADSCs) induced by H₂O₂^[10]. 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^[4].
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^[6].