|
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] |
|