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

et al. 2021

Sci Rep

Soybean meal-induced enteropathy (SBMIE) is prevalent in aquaculture. The aim of this study is to evaluate the role of daidzein on SBMIE of juvenile turbot (Scophthalmus maximus L.) by feeding with fish meal diet (FM), soybean meal diet (SBM, 40% fish meal protein in FM replaced by soybean meal protein) and daidzein diet (DAID, 40 mg/kg daidzein supplemented to SBM) for 12 weeks. We found that daidzein supplementation elevated the gene expression of anti-inflammatory cytokine TGF-β, decreased gene expression of pro-inflammatory cytokines TNF-α and signal molecules p38, JNK and NF-κB. SBM up-regulated the genes expression related to oxidative stress and apoptosis, but dietary daidzein restored it to the similar level with that in FM group. Moreover, dietary daidzein up-regulated gene expression of tight junction protein, and modified the intestinal microbial profiles with boosted relative abundance of phylum Proteobacteria and Deinococcus–Thermus, genera Sphingomonas and Thermus, species Lactococcus lactis, and decreased abundance of some potential pathogenic bacteria. In conclusion, dietary daidzein could ameliorate SBM-induced intestinal inflammatory response, oxidative stress, mucosal barrier injury and microbiota community disorder of turbot. Moreover, p38, JNK and NF-κB signaling might be involved in the anti-inflammatory process of daidzein, and daidzein itself might act as an antioxidant to resist SBM-induced oxidative damage.

Section: Discussionmentioning

confidence: 99%

The protective role of daidzein in intestinal health of turbot (Scophthalmus maximus L.) fed soybean meal-based diets

et al. 2021

Sci Rep

“…NF-κB links inflammation with cancer via the activation of the upstream molecule IKKP, which promotes the development of inflammation-associated tumors. Selectively inhibiting NF-κB activation, will decrease rate of tumor development (41). It has been demonstrated that STAT3 and NF-κB have very important roles in the tumor development process promoted by inflammation.…”

Section: Discussionmentioning

confidence: 99%

Embelin inhibits abdominal aortic aneurysm through decreasing IL‑6‑induced STAT3 and NF‑κB inactivation

Wang

2018

Mol Med Report

The aim of the present study was to investigate the effect of embelin on abdominal aortic aneurysm (AAA). AAA model mice were induced by chronic infusion of 1,000 ng/kg/min Angiotensin II. AAA model mice were treated with 25, 50 or 100 mg/kg embelin for 28 days. Embelin inhibited tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6, IL‑18 and malondialdehyde (MDA) level activities, increased superoxide dismutase, glutathione (GSH) and GSH peroxidase level activities and inhibited MDA level activities in AAA mice Embelin suppressed the secretion of matrix metalloproteinase‑9 protein expression, monocyte chemoattractant protein‑2 activity and epithelial neutrophil‑activating peptide expression levels in AAA mice. Embelin suppressed phosphorylated‑signal transducer and activator of transcription (STAT) 3, phosphorylated‑p38 mitogen‑activated protein kinase and nuclear factor (NF)‑κB protein expression in AAA mice. These findings indicate that embelin inhibits AAA through decreasing IL‑6‑induced STAT3, and NF‑κB inactivation.

“…It has been reported that COX-2 mRNA expression was significantly increased in Ang II-induced AAA mice compared to the control mice. 19 In order to clarify the potential effect of Tregs on COX-2 expression in aortic tissues, immunohistochemical staining was performed in the in vivo experiment. Notably, compared with the control and PBS groups, COX-2 expression was markedly attenuated in Tregs group (P < 0.05, Figure 2A…”

Section: Tregs Transfer Attenuated Cox-2 Expression In Micementioning

confidence: 99%

Regulatory T cells protected against abdominal aortic aneurysm by suppression of the COX‐2 expression

J Cellular Molecular Medi

Kong

et al. 2019

CD4+CD25+ regulatory T cells (Tregs) have been shown to protect against the development of abdominal aortic aneurysm (AAA). Cyclooxygenase‐2 (COX‐2), a pro‐inflammatory protein, can convert arachidonic acid into prostaglandins (PGs). The present study was aimed to investigate the effect of Tregs on COX‐2 expression in angiotension II (Ang II)‐induced AAA in ApoE−/− mice. Tregs were injected via tail vein in every 2 weeks. Ang II was continuously infused by a micropump for 28 days to induce AAA. In vivo, compared with the control group, adoptive transfer of Tregs significantly reduced the incidence of AAA, maximal diameter, and the mRNA and protein expression of COX‐2 in mice. Immunofluorescence showed that Tregs treatment reduced COX‐2 expression both in smooth muscle cells (SMCs) and macrophages in AAA. In vitro, the Western blot analysis showed that Tregs reduced Ang II‐induced COX‐2 expression in macrophages and SMCs. Meanwhile, ELISA showed that Tregs reduced Ang II‐induced prostaglandin E2 (PGE2) secretion. Moreover, Tregs increased SMC viability and induced transition of macrophages phenotype from M1 to M2. In conclusion, Tregs treatment dramatically decreased the expression of COX‐2 in vivo and in vitro, suggesting that Tregs could protect against AAA through inhibition of COX‐2. The study may shed light on the immune treatment of AAA.