TABLE 1.

Some therapeutic applications of curcumin/curcuminoids

Type of biological activity	Therapeutic effectsa	References
Anticancer	Suppress cancer cell proliferation—inhibit NF-κB and consequently downregulate NF-κB-regulated gene products such as COX-2 protein and other proteins that are associated with carcinogenesis, tumor initiation, promotion, and metastasis in a wide variety of cancers	30–40
	Induce apoptosis (programmed cell death type I) by activation of caspase-8, BID cleavage, cytochrome c release, and downregulation of Bcl-2 expression
	Induce autophagy (programmed cell death type II) regulated by simultaneous inhibition of the Akt/mTOR/p70S6K pathway and stimulation of the ERK1/2 pathway
Cholesterol lowering	Decrease LDL cholesterol, total cholesterol, and triglycerides and raise HDL (good) cholesterol	41, 42
	Upregulate CYP7A1, a rate-limiting enzyme in the biosynthesis of bile acid from cholesterol in liver that is involved in the decrease of cholesterol; this induction of CYP7A1 increases the conversion of cholesterol into bile acids and its excretion
Antidiabetic	Suppress expression of hepatic gluconeogenesis genes (PEPCK and G6Pase) similarly to insulin	43–46
	Activate AMPK and downregulate ACC; also implicated in glucose transport and shown to suppress the key gluconeogenic genes PEPCK and G6Pase
Anti-inflammatory	Inhibit NF-кB, COX-2, 5-LOX, iNOS, and other molecules that mediate inflammatory effect	40, 47–52
Antioxidant	Protect biomembranes against lipid peroxidative damage by scavenging the reactive free radicals involved in the peroxidation	31, 49, 50, 53–55
Anti-Alzheimer's disease	Reduce amyloid plaques and accumulated β-amyloid aggregates	56–59
	Suppress pro-oxidant, proinflammatory, and JNK-mediated toxic amyloid aggregate effects
Anti-HIV	Inhibit HIV replication	60–62
	Inhibit HIV-1 and HIV-2 proteases
Wound healing	Protect tissue from oxidative damage due to their antioxidant properties	63, 64
	Increase formation of granulation tissue and biosynthesis of extracellular matrix proteins, especially lower in diabetic wounds
Anti-Parkinson's disease	Reduce aggregation of α-synuclein	65, 66
	Protect dopaminergic neurons from apoptosis by inhibition of JNK

^aNF-κB, nuclear transcription factor κB; COX-2, cyclooxygenase-2; BID, BH3-interacting domain death agonist; LDL, low-density lipoprotein; HDL, high-density lipoprotein; CYP7A1, cholesterol 7a-hydroxylase; 5-LOX, 5-lipoxygenase; iNOS, inducible nitric oxide synthase; JNK, Jun N-terminal kinase.