Pharmacological Effects and Underlying Mechanisms of Licorice-Derived Flavonoids

Table 1

The anti-inflammatory properties of licorice flavonoids in vitro.

Compounds	Dose	Inflammation	Cell line/tissue	Inhibition	References
Licochalcone A	5–20 μM	LPS-induced inflammatory reactions	RAW 264.7 cell	Reduced the concentration of TNF-α, IL-6, and IL-1β	[35]
	3 and 10 μM	LPS-induced inflammatory reactions	RAW 264.7 cell	Dose-dependently inhibited LPS-induced ROS production and reduced the generation of NO, IL-6, and PGE2	[32]
	15 nM	IL-1β-stimulated inflammation	Normal human dermal fibroblasts	Exhibited the 50% inhibition of COX-2-dependent PGE2 production	[36]
	5–20 μM	IL-1β/TNF-α-stimulated inflammation	Primary chondrocytes	Inhibited PGE2, NO, iNOS, COX-2, matrix metalloproteinase-1 (MMP-1), MMP-13, and MMP-3 production in chondrocytes	[37]
Licochalcone C	50 μM	LPS- (10 μg/mL) and interferon-γ (IFN-γ) (20 ng/mL) stimulated inflammation in THP-1 cell	Human myeloid leukemia mononuclear cell (THP-1)	Attenuated inflammatory response by diminishing the expression and activity of iNOS, by modulating extracellular O2^- generation and by restraining the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)	[38]
Isoliquiritigenin	2.5–10 μg/ml	LPS- (0.1 μg/ml) induced proinflammatory mediators production	J774A.1 murine macrophage cell line	Inhibited NO, IL-1β, and IL-6 production dose-dependently	[39]
	10 μM	2,4-Dinitrochlorobenzene (DNCB) induced atopic dermatitis	THP-1 cell line	Suppressed the differentiation of CD54 and CD86 and restrained the activation of extracellular signal-regulated kinase (ERK) and p38-α mitogen-activated protein kinase (p38-α)	[40]
Glabridin	5–10 μg/ml	LPS (0.1 μg/ml) induced proinflammatory mediators production	J774A.1 murine macrophage cell line	Moderate inhibition in NO levels with a maximum inhibition of 33% at the highest tested concentration	[39]
	5–20 μM	LPS (1 μg/mL) stimulated inflammation	HaCaT cell line	At 20 μM, the inhibition reached 47%, 53%, and 68% for IL-1β, IL-6, and p65, respectively; and the suppression reached 53%, 55%, and 45% for IL-17A, IL-22, and IL-23	[41]
	1–10 μM	TNF-α (10^−10 M) induced increase of PGE2 and NO in osteoblasts	MC3T3-E1 cells	The release of PGE2 and the increase of NO in osteoblasts were decreased significantly	[42]
Liquiritin	50 and 100 μM	LPS (100 ng/mL) stimulated microglial cell model	Murine BV2 cell line	Inhibited the increase of NO and proinflammatory mediators iNOS, COX-2, IL-1β, TNF-α, and IL-6	[43]
Liquiritigenin	50 and 100 μM	LPS- (100 ng/mL) induced microglial cell model	Murine BV2 cell line	Suppressed the augment of NO and proinflammatory mediators COX-2, iNOS, IL-1β, IL-6, and TNF-α	[43]
	20 and 40 μM	IL-1β (10 ng/ml) induced inflammation	Chondrocytes from 1-week-old Sprague-Dawley rats	Inhibited the IL-1β-induced expression of NO and PGE2	[44]
Licoricidin	0.5–1 μg/ml	LPS-stimulated secretion of cytokines and MMPs by human monocyte-derived macrophages	Human monoblastic leukemia cell line	Inhibited the secretion of IL-6, chemokine ligand 5, and MMP-7, MMP-8, and MMP-9	[45]