Table 1.
Curcumin inhibits the production and action of TNF in vitro
| Production of TNF |
|---|
| • Inhibited LPS-induced TNF and IL-1 release from macrophages (Chan, 1995). |
| • Inhibited production of IL-8, MIP-1α, MCP-1, IL-1β and TNF-α by PMA- or LPS-stimulated human monocytes and alveolar macrophages (Abe et al., 1999). |
| • Inhibited LPS-induced TNF-α release from macrophages (Jang et al., 2001). |
| • Inhibited the expression/production of IL-12 and TNF-α by peritoneal macrophages (Gao et al., 2004). |
| • Decreased NF-κB activation and TNF-α secretion after LPS exposure in U-937 cells (Strasser et al., 2005). |
| • Inhibited the production of IL-1, IL-6 and TNF-α in LPS-stimulated BV2 microglia (Jin et al., 2007). |
| • Exhibited neuroprotective effects through suppression of NO, TNF-α, IL-1α and IL-6 from Abeta (25–35)/IFN-γ- and LPS-stimulated microglia cells (Lee et al., 2007). |
| • Inhibited inflammatory responses of adipose tissue in obesity by suppressing release of TNF-α, NO and MCP-1 from adipocytes (Woo et al., 2007). |
| • Inhibited NO and TNF-α production in rat primary microglia induced by LPS (Zhang et al., 2008). |
| • Inhibited LPS-induced TNF-α and IL-6 synthesis in macrophages (Liang et al., 2008). |
| • Down-regulated TNF, IL-1, NO and PGE2 in Raw 264.7 cells possibly through induction of phase II/antioxidant enzymes including HO-1 and NQO-1 (Cheung et al., 2009). |
| • Reversed palmitate-induced insulin resistance through suppression of NF-κB, TNF-α and IL-6 in adipocytes (Wang et al., 2009). |
| • Inhibited LPS-induced production of TNF-α, IL-1β, MCP-1, COX-2, iNOS and p65 NF-κB in the macrophages (Liang et al., 2009). |
| • Inhibited the high glucose-induced secretion of IL-6, IL-8, MCP-1 and TNF-α in U937 monocytes (Jain et al., 2009). |
| • Inhibited secretion of TNF-α and IL-6 in vitro (Tham et al., 2010). |
| • Inhibited the release of TNF-α and IL-6 in LPS-stimulated RAW 264.7 macrophages (Zhao et al., 2010). |
| • Inhibited IκB phosphorylation, NF-κB activation and TNF-α production induced by LPS in mouse macrophages (Nishida et al., 2010). |
| • Decreased LPS-induced TNF-α and IL-1β expression at both transcriptional and protein level in microglial cells (Zhang et al., 2010a). |
| Action of TNF-α |
|---|
| • Inhibited TNF-induced NF-κB activation in human myeloid cells (Singh and Aggarwal, 1995). |
| • Reduced TNF-induced endothelial tissue factor by inhibiting AP-1 and NF-κB in endothelial cells (Bierhaus et al., 1997). |
| • Blocked the activation of AP-1 and NF-κB induced by IL-1α and TNF-α in stromal cells (Xu et al., 1997). |
| • Inhibited TNF-α-induced expression of ICAM-1, VCAM-1 and E-selectin in HUVEC (Gupta and Ghosh, 1999; Kumar et al., 1998). |
| • Suppressed TNF-α-induced VEGF secretion in U937 and Raji cells. Reduced the expression of VEGF165 and VEGF121 mRNA induced by TNF-α (Chen et al., 2005). |
| • Inhibited TNF-mediated constitutive NF-κB activation linked to proliferation of mantle cell lymphoma cells (Shishodia et al., 2005). |
| • Blocked TNF-α-induced endothelial dysfunction in HUVEC (Nan et al., 2005). |
| • Down-regulated TNF-induced expression of cell proliferation and anti-apoptotic and metastatic gene products (Aggarwal et al., 2006). |
| • Inhibited TNF-α-stimulated Gb3 synthase (GalT6) mRNA expression in intestinal epithelial cells (Moon et al., 2006). |
| • Inhibited TNF-α-induced expression of IL-1β, IL-6, TNF-α and cyclin E, but not IL-8, in HaCaT cells (Cho et al., 2007). |
| • Inhibited TNF-α-induced NF-κB activation in MCF-7 cells by inhibiting the proteasomal activities (Yoon and Liu, 2007). |
| • Suppressed TNF-α-induced expression of ICAM-1 and VCAM-1, and secretion of IL-6, IL-8 and MCP-1 in HUVEC (Kim et al., 2007). |
| • Inhibited TNF-α-induced NF-κB activation in chronic myeloid leukaemia cells through modulation of redox status of the cells (Sandur et al., 2007). |
| • Down-regulated the expression of 29 out of 84 TNF-α-activated NF-κB-associated genes in leukaemia cells (Reuter et al., 2009). |
| • Inhibited TNF-induced NF-κB activation in leukaemia cells (Yadav et al., 2010). |
| • Inhibited TNF-α-induced cell migration, intracellular ROS generation, MMP-9 expression, MMP-9 activity and NF-κB in human aortic smooth muscle cells (Yu and Lin, 2010). |
| • Attenuated TNF-α-induced enhancement of TRPC1 expression, and COX-2-dependent PGE2 production in colonic myofibroblasts (Hai et al., 2011). |
| • Inhibited NF-κB-mediated inflammation in human tenocytes through suppression of the PI3K/Akt pathway (Buhrmann et al., 2011). |
AKT, AKT8 virus oncogene cellular homologue; AP-1, activator protein-1; HO-1, haeme oxygenase-1; ICAM-1, intercellular adhesion molecule-1; MCP-1, monocyte chemotactic protein-1; MIP-1α, macrophage inflammatory protein-1α; MMP-9, matrix metallopeptidase-9; NQO1, NADH quinone oxidoreductase 1; TRPC1, transient receptor potential channel 1; VCAM-1, vascular cell adhesion molecule-1.