Table 1.
Component | Effects | Mechanisms |
---|---|---|
Puerarin | Alzheimer’s disease | Antioxidant |
Parkinson disease | Increases the expression of TH and decreases the expression of GFAP; ameliorated MPTP-induced ROS formation | |
Ischemic stroke | Decreases the level of serum vWF and sTM; increases the expression of BDNF and activates PI3K/AKT and MAPK/ERK signaling pathways | |
Vascular dementia | Antioxidant | |
Myocardial hypertrophy | Through (AMPK)/target of rapamycin (mTOR)-mediated signaling pathway; inhibits activation of the redox-sensitive p38 and the NF-κB pathway; blocks Rac1-dependent NADPH oxidase activation; blocks PI3K/Akt and JNK signaling pathways | |
Hypertension | Improves EDR; increases the phosphorylation of eNOS and decreases the expression of gp91phox, p22phox, TGFβ1, and VCAM-1; reduces the expression of TGF-β and Smad3 mRNA and increases the expression of Smad7 mRNA | |
Angina pectoris | Inhibits the expression of the protein and mRNA levels of CRP | |
Acute myocardial ischemia | Decreases the upregulation of P2X3 mRNA and protein levels; opens the calcium-activated potassium channel and activates protein kinase C; increases NO concentration; antioxidant | |
Diabetic retinopathy | Alleviates cell apoptosis; attenuates IL-1β-mediated leukostasis | |
Diabetic nephropathy | Regulates the expression of glomerular extracellular matrix | |
Osteoporosis | Promotes the serological level of osteocalcin, BMSC proliferation, the expression of ALP, and suppresses the serological level of adiponectin and adiposity | |
Hyperlipidemia | Enhances the expression of 7alpha-hydroxylase (CYP7A1) mRNA and promotion of cholesterol and bile acids excretion in liver | |
Digestive system cancer | Induces the loss of MMP and generation of ROS | |
Breast cancer | Downregulates MDR1 expression | |
Genistein | Ischemic stroke | Antioxidant; enhances eNOS phosphorylation/activation and NO-mediated thiol modification of Keap1; decreases thromboxane A2 concentration and leukocyte-platelet aggregates production |
Myocardial hypertrophy | Regulates the MTA3/TAK1/MKK4/JNK signaling pathway | |
Hypertension | Regulates the activity of eNOS and reverse endothelial dysfunction | |
Diabetes | Improves islet cell survival and proliferation and facilitates insulin production; activates the cAMP/PKA-dependent extracelluar ERK1/2 signaling pathway; antioxidant; improves high glucose-impaired intracellular cAMP production and PKA activity | |
Osteoporosis | Improves the balance between RANKL and its decoy receptor OPG | |
Hyperlipidemia | Upregulates the expression of hepatic LDL receptor, estrogen receptor α(ERα), and ERβ mRNAs; lowers the levels of the plasma lipid and vWF | |
Digestive system cancer | Inhibits phosphorylation of AKT and induces the mitochondrial pathway of apoptosis; inhibits β-catenin target genes | |
Reproductive system cancer | Suppresses EMT and the migration capacities of BG-1 ovarian cancer cells via ER signaling and the downregulation of TGF-β signal | |
Breast cancer | Activates ATR kinase and BRCA1 complex; downregulates microRNA-155 | |
Daidzein | Hyperlipidemia | Enhances the cholesterol homeostasis genetic program; inhibits the activity of pancreatic lipase and lipoprotein lipase and the differentiation of rat preadipocytes |
Diabetes | Activates AMP-activated protein kinase (AMPK) |
TH: Tyrosine hydroxylase, GFAP: Glial fibrillary acidic protein, MPTP: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, ROS: Reactive oxygen species, vWF: von Willebrand factor, sTM: Thrombomodulin, BDNF: Brain-derived neurotrophic factor, AMPK: 5’-adenosine monophosphate kinase, CRP: C-reactive protein, BMSC: Bone marrow stromal cell, ALP: Alkaline phosphatase, MMP: Matrix-metalloproteinases, OPG: Osteoprotegerin, EMT: Epithelial-mesenchymal transition, JNK: Jun N-terminal kinase, EDR: Endothelium-dependent relaxation, ATR: Ataxia telangiectasia-mutated and Rad3-related, NOS: Nitric oxide synthase, RANKL: Receptor activator of NF-κB ligand, TNF: Tumor necrosis factor, IL: Interleukin