Therapeutic potential of curcumin in digestive diseases

Table 1 Pharmacokinetics parameters in healthy volunteers after administration of curcuminphytosomes or unformulated curcumin

Curcuminoid	Formulation	AUC (ng/mL)	Cmax (ng/mL)	tmax (h)	Relative absorption2
Curcumin (1a)	Curcuminphytosome high	538.0 ± 130.7	50.3 ± 12.7	3.8 ± 0.6	19.21
	Curcuminphytosome low	272.6 ± 68.52	24.2 ± 5.9	4.2 ± 0.8	17.53
	Reference	122.5 ± 29.3	9.0 ± 2.8	6.9 ± 2.2	1
Demethoxycurcumin (1b)	Curcuminphytosome high	655.0 ± 195.7	134.6 ± 40.6	2.4 ± 0.3	68.34
	Curcuminphytosome low	297.4 ± 107.3	39.1 ± 11.4	3.1 ± 0.4	55.54
	Reference	55.8 ± 15.5	4.2 ± 1.1	4.4 ± 1.0	1
Bisdemethoxycurcumin (1c)	Curcuminphytosome high	142.2 ± 58.2	24.9 ± 8.1	2.2 ± 0.4	56.85
	Curcuminphytosome low	70.1 ± 34.3	8.8 ± 3.1	2.4 ± 0.6	53.15
	Reference	24.6 ± 10.3	2.1 ± 0.8	3.4 ± 1.2	1
Total curcuminoids	Curcuminphytosome high	1336.0 ± 357.1	206.9 ± 54.9	2.7 ± 0.3	31.56
	Curcuminphytosome low	640.2 ± 197.7	68.9 ± 16.9	3.3 ± 0.3	27.26
	Reference	202.8 ± 53.8	14.4 ± 4.2	6.9 ± 2.2	1

¹Actual results not baseline subtracted, and errors are standard error of the mean ± SE;

²Area under the curve (AUC) normalized;

³Average: 18.3;

⁴Average: 61.9;

⁵Average: 54.1;

⁶Average: 29.l4.

Table 2 Curcumin’s anti-inflammatory and anticancer effects

Anti-inflammatory effects	Anticancer effects
Downregulation of NF-κB,	Inhibition of carcinogen activation
Inhibition, via NF-κB, of COX-2, lipoxygenase, and iNOS enzymes	Stimulation of carcinogen detoxification
Inhibition of the inflammatory cytokines, such as TNF-α, interleukin (IL)-1, -2, -6, -8, and -12, MCP, and migration inhibitory protein	Suppression of pro-inflammatory signaling
Inhibition of PPAR-g	Inhibition of STAT
	Induction of cancer cell apoptosis cell cycle arrest
	Inhibition of angiogenesis and metastasis
	Modulation of oncogenes and tumor suppressor genes

TNF-α: Tumor necrosis factor-α; MCP: Monocyte chemoattractant protein; PPAR-g: Peroxisome proliferator-activated receptor-g; iNOS: Inducible nitric oxide synthase; STAT: Signal transducer and activator of transcription; NF-κB: Nuclear factor kappa B; COX-2: Cyclooxygenase-2.

Table 3 Substances and hepatic intoxication mechanisms contrasted by curcumin

Intoxications	Pathogenetic mechanisms	Curcumin effects
Iron (alcoholic liver disease; steatosis, viral hepatitis; anemia)	Fibrosis induced by oxidation	Anti-oxidant enzymatic activity
Alcohol (chronic or acute intoxication)	Phospholipase A2 activation	Phospholipase A2 inhibition by NF-κB
High-fat diet (lipid storage)	Focal degeneration, micronecrosis	Acil-CoA, cholesterol biliary acids; LDL peroxidation
Xenobiotics induced acute damage	ROS, lipid peroxidation, inflammation	Scavenger activity on NF-κB; anti-oxidant enzymatic activity
Xenobiotics induced chronic damage	Inflammation and hepatocellular necrosis	Hepatic fibrosis inhibition by NF-κB
Poisons (carbon tetrachloride)	Inflammatory self-maintenance	Hepatic inflammation inhibition by NF-κB

ROS: Reactive oxygen species; LDL: Low density lipoprotein; NF-κB: Nuclear factor kappa B.