Table 1.
•Curcumin was more active than THC in suppressing carrageenin-induced inflammation [21]. |
•Curcumin was more effective than THC in preventing PMA-induced skin tumor promotion in mice [22]. |
•Curcumin was more effective than THC as an antioxidant [23]. |
•Under aerated conditions, curcumin was more active than THC [24]. |
•Curcumin was more effective than THC in suppressing NF-κB activation [19,25,26]. |
•Curcumin was more effective than THC in down-modulating PMA-induced COX2 expression and PGE2 production [15]. |
•Curcumin was more effective than THC in inhibiting 5-LOX activity [27]. |
•Curcumin was more active than THC in ROS production and as a membrane mobility coefficient [28]. |
•Curcumin was more effective than THC in modulating ABC drug transporters [29]. |
•Curcumin induced apoptosis of HL-60 (decrease of bcl-2; increase of bax) but THC did not [30]. |
•Curcumin induced HO-1 expression through activation of ARE but THC did not [31]. |
During induction of cell death, curcumin induced ROS and GSH; THC did not [32] |
•Curcumin, but not THC, inhibited NO production and iNOS expression [26]. |
•Curcumin was more effective than THC in inhibiting the Wnt/beta-catenin pathway by decreasing the amount of the transcriptional coactivator p300 [33,34]. |
•Curcumin, but not THC, inhibited LPS-stimulated NF-κB and COX-2 gene expression [35]. |
•Curcumin, but not THC, was effective in reducing amyloid plaque burden and amyloid aggregation [36]. |
•Curcumin, but not THC, induced HO-1 expression and Nrf2 nuclear translocation [37] |
•Curcumin, but not THC, covalently blocked the catalytic thiolate of C1226 of DNMT1 [38]. |
•Curcumin, but not THC, inhibited Ca(2+) influx through CRAC for activating immune cells [39]. |
•Curcumin was more effective than THC in inducing FOXO3a-mediated gene expression by inducing FOXO3a phosphorylation and nuclear translocation [40]. |
•Curcumin was more effective than THC in reducing β-amyloid and phosphorylated Tau protein burden in Alzheimer transgenic mice [41]. |
•Curcumin was more active than THC in suppressing LPS-induced production of TNF-α [42]. |
•Curcumin, but not THC, inhibited entry of hepatitis C virus genotypes into human liver cells [43]. |
•Curcumin, but not THC, was taken up and increased lipid accumulation in monocytic cell line THP-1 [44]. |
•Curcumin was more effective than THC in inhibiting TNF-induced expression of cyclin D1 and VEGF [25]. |
•Curcumin inhibited type A influenza virus infection to a greater extent than THC by interfering with viral hemagglutination activity [45]. |
•Curcumin inhibited IKK1 and IKK2 activities induced by LPS to a greater extent than THC [19]. |
PMA, phorbol 12-myristate 13-acetate; NF-κB, nuclear factor-kappaB; COX2, cyclooxygenase-2; PGE2, prostaglandin E2; 5-LOX, 5-lipoxygenase; HAT, histone acetyltransferase; THC, tetrahydrocurcumin; HO-1, heme oxygenase 1; ARE, antioxidant response element; ROS, reactive oxygen species; GSH, glutathione; iNOS, inducible nitric oxide synthase; Nrf2, nuclear factor erythroid 2 [NF-E2]-related factor 2; LPS, lipopolysaccharides; DNMT1, DNA (cytosine-5)-methyltransferase 1; CRAC, Ca(2+)-release activated Ca(2+) channels; FOXO3a, Forkhead box O3a; TNF-α, tumor necrosis factor alpha; VEGF, vascular endothelial growth factor; IKK, IkappaB kinase.