ABSTRACT
Vitexin (VIT) is a dietary polyphenol that belongs to the group of c-glycosylated flavonoids and is widely found in food and medicinal plants such as mung bean and hawthorn. Numerous studies have confirmed that VIT has extensive pharmacological activities with protective effects against a variety of diseases. With the great attention given to VIT, more and more studies have begun to look at its relationship to liver disease, but a comprehensive summary of this content is still lacking. Therefore, this review summarizes the protective effects of VIT on various liver diseases. In addition, the toxicological properties and pharmacokinetic profile of VIT are discussed to provide a basis for further development and expansion of its health effects.
Abbreviations
VIT | = | Vitexin |
ROS | = | reactive oxygen species |
ALD | = | alcoholic liver disease |
NAFLD | = | non-alcoholic fatty liver disease |
NASH | = | non-alcoholic steatohepatitis |
MAFLD | = | metabolic dysfunction associated fatty liver disease |
HCC | = | hepatocellular carcinoma |
FAO | = | fatty acid oxidation |
SREBP-1c | = | sterol regulatory element-binding protein-1c |
ACC | = | acetyl-CoA carboxylase |
FAS | = | fatty acid synthase |
HFD | = | high-fat diet |
PPAR | = | peroxisome proliferator-activated acceptor |
CPT | = | carnitine palmitoyl transferase |
AMPK | = | AMP-activated protein kinase |
HMG CoA | = | beta-hydroxy beta methyl glutamyl- coenzyme A |
TG | = | triglycerides |
TC | = | total cholesterol |
LDL | = | low-density lipoprotein |
SOD | = | superoxide dismutase |
CAT | = | catalase |
GSH-Px | = | glutathione peroxidase |
OA | = | oleic acid |
Nrf2 | = | nuclear factor E2-related factor 2 |
HO-1 | = | heme oxygenase-1 |
T-AOC | = | total antioxidant capacity |
ER | = | endoplasmic reticulum |
FOXO | = | forkhead box O |
TLRs | = | liver toll-like receptors |
NF-κB | = | NF-kappa B |
TNF-α | = | tumor necrosis factor |
IL-6 | = | interleukin-6 |
IL-1β | = | interleukin-1β |
IRS | = | insulin receptor substrate |
Glut4 | = | glucose transporter |
AKT | = | protein kinase B |
InsR | = | insulin receptor |
mTOR | = | mechanical target of rapamycin |
SIRT1 | = | Sirtuin1 |
MDA | = | malondialdehyde |
Bcl-2 | = | B-cell lymphoma-2 |
AST | = | aspartate transaminase |
ALT | = | alanine aminotransferase |
DILI | = | drug-induced liver injury |
APAP | = | acetaminophen |
AIH | = | autoimmune hepatitis |
GSK-3β | = | glycogen synthase kinase 3β |
SD | = | Sprague-Dawley |
LDH | = | lactate dehydrogenase |
Bax | = | Bcl-2-associated X |
CCl4 | = | carbon tetrachloride |
D-Gal N | = | D-galactosamine |
HSC | = | hepatic stellate cell |
CLD | = | cholestatic liver disease |
GCDC | = | glycine chenodeoxycholic acid |
JAK2 | = | janus kinase 2 |
STAT3 | = | signal transducer and activator of transcription 3 |
JNK | = | c-Jun N-terminal kinase |
MAPKs | = | mitogen-activated protein kinases |
AIH | = | autoimmune hepatitis |
Tmax | = | maximum peak time |
Cmax | = | peak concentration |
AUC | = | area under the curve |
Papp | = | apparent permeability coefficient |
CLs | = | clear compounds |
MRT | = | mean retention time |
UGT | = | uridine diphosphate glucuronosyltransferase |
β-CD | = | β-cyclodextrin |
MI | = | myocardial ischemia |
Disclosure statement
No potential conflict of interest was reported by the author(s).
Author contributions
SD, Writing – review & editing, Writing – original draft, Investigation; KF, Writing – review & editing; YF L, Writing – original draft, Data curation; YX Y, Data curation; FZ, Resources; RW, Resources; YL G, Validation; CH Y, Validation; YX L, Conceptualization, Supervision, Funding acquisition*.