Table 2.
Curcumin inhibits TNF production in animals
| • Prevented alcohol-induced liver disease in rats by inhibiting the expression of NF-κB-dependent genes including TNF-α (Nanji et al., 2003). |
| • Reduced the serum level of TNF-α and NO in B16F-10 melanoma cells bearing C57BL/6 mice (Leyon and Kuttan, 2003). |
| • Suppressed the myocardial TNF-α and MMP-2 expression and improved left ventricular function in pressure overloaded rabbits (Yao et al., 2004). |
| • Decreased the elevations in plasma IL-8, IL-10 and TNF-α in rabbits after cardiopulmonary bypass and cardiac global ischaemia (Yeh et al., 2005). |
| • Significantly lowered the serum TNF-α and IL-6 levels in rat model of acute pancreatitis (Gulcubuk et al., 2006). |
| • Decreased the expression of TNF-α and reduced the mortality in rat model of sepsis (Siddiqui et al., 2006). |
| • Reduced the mortality rate of LPS-infused rats by decreasing the circulating TNF-α levels and the consumption of peripheral platelets and plasma fibrinogen (Chen et al., 2007). |
| • Significantly inhibited TNF-α and NO levels in rat model of diabetic neuropathy (Sharma et al., 2007b). |
| • Down-regulated the expressions of TNF-α and IL-8 in the copper-overloaded rats (Wan et al., 2007). |
| • Decreased the levels of NO, TGF-β1 and TNF-α in rat model of hepatic fibrosis (Shu et al., 2007). |
| • Inhibited expression of TNF-α and IL-1β stimulated by LPS in murine macrophages through inhibition of NF-κB pathway (Chen et al., 2008). |
| • Significantly reduced the LPS-induced overproduction of circulating TNF-α, IL-1β and IL-6, brain glutamate, PGE2, and hydroxyl radicals in rabbit (Huang et al., 2008). |
| • Significantly decreased TNF-α mRNA and caspase-8 that probably contributes to the protective role of the turmeric-based diet against renal injury in rat (Hashem et al., 2008). |
| • Reduced TNF-α levels in a rabbit model of non-alcoholic steatohepatitis (Ramirez-Tortosa et al., 2009). |
| • Decreased the levels of TNF-α in a rat model of subchronic inflammation (Nandal et al., 2009). |
| • Exhibited anti-fibrosis activity by decreasing the levels of TNF-α and TGF-β1 in serum and lung tissue of SiO2-induced fibrosis mice model (Jiang et al., 2009). |
| • Prevented the injurious effects of DSS and ameliorated release of TNF-α and NO in a rat model (Arafa et al., 2009). |
| • Decreased serum levels of IL-12 and TNF-α in mice infected with Schistosoma mansoni cercariae (Allam, 2009). |
| • Significantly attenuated oxidative stress and TNF-α levels in a mouse model of immunologically induced fatigue (Gupta et al., 2009). |
| • Significantly decreased the blood levels of IL-6, MCP-1, TNF-α, glucose, HbA1 and oxidative stress in streptozotocin-induced diabetic rat model (Jain et al., 2009). |
| • Decreased LPS-induced TNF-α production in lungs of mice. At 5% concentration, curcumin significantly improved survival of mice and decreased radiation-induced lung fibrosis (Lee et al., 2010). |
| • Exhibited protective effects against necrotizing enterocolitis in neonatal rats, possibly by inhibiting COX-2, reducing TNF-α and increasing IL-10 contents (Jia et al., 2010). |
| • Significantly decreased the levels of TNF-α and IL-8 in the serum and prostate tissues in a rat model of prostatitis (Zhang et al., 2010b). |
| • Significantly decreased the production of TNF-α in a mouse model of acute inflammation (Bansal and Chhibber, 2010). |
| • Protected mice from LPS/GalN-induced hepatic injury and inflammation by blocking TNF-α production (Yun et al., 2010). |
| • Increased IFN-γ, IL-12 and IL-13 levels, but decreased TNF-α level in rats intoxicated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (Ciftci et al., 2010). |
| • Lowered the production of IL-23p19, IFN-γ, TNF-α, IL-6 and MCP-1 in a murine model of hyperacute Th1-type ileitis (Bereswill et al., 2010). |
| • Suppressed LPS stimulated TNF-α production in mice (Nishida et al., 2010). |
| • Reduced the aluminum-induced inflammatory response as indicated by down-regulation of NF-κB and TNF-α in glial cells (Sood et al., 2011). |
| • Improved the lipid metabolism and delayed the progression of hepatic fibrosis in rats with experimental steatohepatitis through suppression of TNF-α, NF-κB and HMG-CoA reductase (Zeng et al., 2011). |
| • Inhibited mRNA expression of TNF-α in a murine model of asthma (Ammar el et al., 2011). |
| • Suppressed inflammation by reducing levels of TNF-α, NF-κB and IL-6 in CCl4-treated rats (Bassiouny et al., 2011). |
| • Reduced cardiac inflammation through suppression of IL-1β, TNF-α, GATA-4 and NF-κB in a rat model of experimental autoimmune myocarditis (Mito et al., 2011). |
| • Suppressed serum levels of TNF-α and IL-1β in a streptozotocin-induced diabetic mouse model (El-Azab et al., 2011). |
| • Attenuated TNF-α levels and exhibited anti-hyperglycaemic effect and improved insulin sensitivity in high-fat diet-fed rats (El-Moselhy et al., 2011). |
| • Prevented deterioration of the bone structure and produced beneficial effects in bone turnover in transgenic mice possibly through modulation of TNF-α and IL-6 (Yang et al., 2011). |
| • Protected against ischaemia/reperfusion injury in rat skeletal muscle through inhibition of plasma TNF-α levels (Avci et al., 2012). |
| • Inhibited the high glucose-induced plasma TNF-α production and macrophage infiltration and prevented renal injury in diabetic rats (Pan et al., 2012). |
| • Attenuated concanavalin A-induced liver injury in mice by inhibition of TNF expression through TLR-2, TLR-4 and TLR-9 expression (Tu et al., 2012). |
CCl4, carbon tetrachloride; DSS, dextran sulfate sodium; GalN, d-galactosamine; HbA1, haemoglobin α1; HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme A; MCP-1, monocyte chemotactic protein-1; SiO2, silicon dioxide.