Daidzein attenuates abdominal aortic aneurysm through NF-κB, p38MAPK and TGF-β1 pathways

Abstract

The current study focuses on the protection of daidzein on nerves, as daidzein was demonstrated to have a protective effect on neurons of the central nervous system in a glutamate excitotoxicity and oxygen/glucose deprivation model. However, the effect of daidzein on the abdominal aortic aneurysm (AAA) remains unclear. The angiotensin II-induced AAA mouse model was utilized in the present study to determine the effect of daidzein on AAA. The results demonstrated that daidzein significantly attenuated incidence of AAA, max aortic aneurysm and mortality in the angiotensin II-induced AAA mice. Daidzein had an anti-inflammatory effect by inhibiting tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and nuclear factor κB (NF-κB) protein expression. In addition, daidzein strongly suppressed the gene expression of cyclooxygenase (COX)-2, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinase 1 (TIMP-1), transforming growth factor β1 (TGF-β1), and inhibited inducible nitric oxide synthase (iNOS) protein expression in angiotensin II-induced AAA mice. It also inhibited phosphorylation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway. These results demonstrate, to the best of our knowledge for the first time, that the anti-inflammatory effects and inhibitory mechanism of daidzein attenuates AAA in angiotensin II-induced mice. Daidzein contains strong anti-inflammatory activity and affects various mechanism pathways including the NF-κB, p38MAPK and TGF-β1 pathway.