title: Genistein suppresses LPS-induced inflammatory response through inhibiting NF-κB following AMP kinase activation in RAW 264.7 macrophages.
abstract: Genistein, the major isoflavone in soybean, was recently reported to exert beneficial effects in metabolic disorders and inflammatory diseases. In the present study, we investigated the effects and mechanisms of a dietary concentration of genistein on the inflammatory response in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Our results demonstrated that genistein effectively inhibited the LPS-induced overproduction of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), as well as LPS-induced nuclear factor kappa B (NF-κB) activation. In addition, the data also showed that genistein prevented LPS-induced decrease in adenosine monophosphate-activated protein kinase (AMPK) phosphorylation. These effects were obviously attenuated by an AMPK inhibitor. Taken together, our results suggest that the dietary concentration of genistein is able to attenuate inflammatory responses via inhibition of NF-κB activation following AMPK stimulation. The data provide direct evidence for the potential application of low concentrations of genistein in the prevention and treatment of inflammatory diseases.
authors.affiliation: Guangdong Provincial Institute of Public Health, Guangzhou, China.
authors.forename: Guiyuan
authors.initials: G
authors.lastname: Ji
authors.forename: Yupei
authors.initials: Y
authors.lastname: Zhang
authors.forename: Qinhe
authors.initials: Q
authors.lastname: Yang
authors.forename: Shaobin
authors.initials: S
authors.lastname: Cheng
authors.forename: Jing
authors.initials: J
authors.lastname: Hao
authors.forename: Xihong
authors.initials: X
authors.lastname: Zhao
authors.forename: Zhuoqin
authors.initials: Z
authors.lastname: Jiang
mesh_terms: D000263:Adenylate Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000620:Aminoimidazole Carboxamide / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D019833:Genistein / Q000494:pharmacology*; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D011720:Pyrazoles; D011743:Pyrimidines; D012265:Ribonucleotides / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D047428:Protein Kinase Inhibitors; D011720:Pyrazoles; D011743:Pyrimidines; D012265:Ribonucleotides; D014409:Tumor Necrosis Factor-alpha; C516138:dorsomorphin; D000620:Aminoimidazole Carboxamide; D019833:Genistein; D000263:Adenylate Kinase; C031143:AICA ribonucleotide