From:  Genistein as a multi-target therapeutic: translational advances in inflammation and cancer

 Anti-inflammatory effects of genistein.

Mechanism/PathwayInflammatory condition/modelStudy typeReferences
NF-κB inhibition results in a reduction of TNF-α, IL-6, and IL-1βRheumatoid arthritis, lipopolysaccharide (LPS)-stimulated macrophagesIn vitro, in vivo[1, 2]
MAPK pathway suppression (ERK, JNK, p38)Colitis, LPS-induced inflammationIn vitro, in vivo[1, 6]
JAK/STAT signalling modulationAutoimmune disorders, cancer-related inflammationIn vitro[59]
COX-2 and iNOS downregulation results in a reduction of prostaglandin and NOOsteoarthritis, inflammatory bowel diseaseIn vitro, in vivo[2, 14]
Inhibition of TLR4 signalling results in a reduction in MyD88/NF-κB pathway activationSepsis, LPS-challenged modelsIn vitro, in vivo[61]
Antioxidant-mediated inflammation reduction (ROS scavenging, Nrf2 activation)Neuroinflammation, cardiovascular inflammationIn vitro, in vivo[1, 12]
Modulation of inflammasome activation (NLRP3)Liver inflammation, metabolic syndromeIn vitro[62]

COX-2: cyclooxygenase-2; ERK: extracellular signal-regulated kinase; iNOS: inducible nitric oxide synthase; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; NF-κB: nuclear factor-kappa B; ROS: reactive oxygen species; TLR4: Toll-like receptor 4.