Pharmacological Effects and Underlying Mechanisms of Licorice-Derived Flavonoids

Table 4

The antioxidant properties of licorice flavonoids.

Compounds	Model	Dose and effects	References
Isoliquiritigenin	LPS-induced acute lung injury mice	Treatment with isoliquiritigenin (30 mg/kg) enhanced the production of ROS, MPO, and MDA, ameliorating low expression of GSH and SOD caused by LPS stimulation	[148]
	LPS-induced cognitive impairment rats	Isoliquiritigenin (20 mg/kg) pretreatment appeared antioxidant capacity through reversing the downregulation of SOD and GSH-PX activity and reducing the content of MDA	[149]
	Streptozotocin (STZ) induced diabetic retinopathy	Isoliquiritigenin (20 mg/kg/day) treatment markedly reduced diabetes-induced lipid peroxidation by 27.8%, upregulated retinal GSH 1.57-fold, and restored total retinal antioxidant capacity 2.15-fold	[150]
	Caenorhabditis elegans	Isoliquiritigenin (50 μg/ml) reduced heat shock protein-16.2 (HSP-16.2) expression level by 30.8% under mild oxidative stress and increased the survival rate of C. elegans from 10.8% of control group to 97.4% under lethal oxidative stress	[151]
Liquiritigenin	Serum deprivation in HepG2, H4IIE, and AML12 cells induced oxidative stress	Mitochondrial dysfunction, oxidative stress like ROS formation, and resultant cell death caused by nutrition deprivation were prohibited by liquiritigenin (100 μM) pretreatment	[152]
	Citrinin (CTN) induced, oxidative-stress-mediated disruption of embryonic development in mouse blastocysts	CTN-triggered ROS generation for sequent apoptosis and injury of blastocysts was restrained by the preincubation of liquiritigenin (20–40 μM)	[153]
Glabridin	Methotrexate (MTX) triggered liver injury	Glabridin (20 or 40 mg/kg) lower oxidative stress stimulated by MTX through upregulation of MDA level, as well as reduction of GSH level and SOD activity	[154]
	Diabetic vascular complications mouse	Glabridin prevented the antiatherogenic capacity of paraoxonase 2 (PON2) by the interaction of glabridin-PON2 that protected PON2 from oxidation	[155]
Licochalcone A	HepG2 cell and L-02 cell	Licochalcone A inhibited peroxyl radical-induced oxidation of DCFH to DCF in HepG2 cells in a dose-dependent manner and upregulated protein expression of SOD1, CAT, and GPx1 at 2–8 μg/ml	[74]