Fig 1: Effects of resveratrol and pterostilbene on NRF2 nuclear translocation (a) and the protein expression of KEAP1 (b), NQO1 (c), HO1 (d), SOD1 (e), and SOD2 (f) in the jejunum of piglets. The column and its bar represent the mean value and standard error (n = 6 piglets/group), respectively. aOne-way ANOVA test. bNon-parametric Kruskal-Wallis test. HO1 heme oxygenase 1, KEAP1 Kelch ECH associating protein 1, NQO1 NAD(P)H quinone dehydrogenase 1, NRF2 nuclear factor erythroid 2-related factor 2, SOD1 superoxide dismutase 1, SOD2 superoxide dismutase 2, SR-CON piglets continued to be nursed by sows aged between 21 and 28 days, W-CON piglets were fed a basal diet aged between 21 and 28 days, W-RSV piglets were fed a diet supplemented with 300 mg/kg of resveratrol aged between 21 and 28 days, W-PT piglets were fed a diet supplemented with 300 mg/kg of pterostilbene aged between 21 and 28 days
Fig 2: SKI and three anthraquinones including chrysophanol, emodin, and rhein activated the anti-inflammatory and anti-oxidative Keap1/Nrf2 signaling pathway in the adenine-induced CRF rats. (A) Protein expressions of nuclear translocation of Nrf2 and its repressor, Keap1, and its downstream gene products including HO-1, catalase, GCLC, and NQO-1 of the kidney tissues in the different groups. (B) Quantitative analysis of anti-inflammatory and anti-oxidative protein expressions of the kidney tissues in the different groups. ** p < 0.01 compared with the CTL group; # p < 0.05, ## p < 0.01 compared with the CRF group. (C) Immunohistochemical analysis with anti–HO-1 of the kidney tissues in the different groups. Scale bar, 40 µm.
Fig 3: Effect of lucidone on the expression of Nrf2 in DENV-infected cells. Lucidone activated Nrf2 expression and the efficacy of nucleus translocation. (A) DENV-infected Huh-7 cells were treated with the indicated concentrations of lucidone. The cell lysate was separately extracted from the cytoplasm and nuclear extracts and analyzed by western blotting using anti-Bach1, anti-keap1, anti-Nrf2, anti-GAPDH, and anti-LaminB1 antibodies. GAPDH and Lamin B protein levels showed equal loading of cell lysates. (B) DENV-infected cells were transfected with reporter plasmid p3xARE-Luc and treated with the indicated concentrations of lucidone for 3 days, and total cell lysates were analyzed for luciferase activity. “0” indicates treatment with 0.1% DMSO. The luciferase activity was presented as fold changes compared to that in lucidone-untreated cells, in which the level was presented as 1. Results are expressed as mean ± SD (error bar) of three independent experiments. *P versus lucidone non-treated control group; #P versus DENV-infected control group.
Fig 4: The relative mRNA expression of Keap1, Nrf2, Nqo1, and Ho1 in intestinal porcine jejunal epithelial cells (IPEC-J2) exposed to ZEA at concentrations of 0, 10, 20, and 40 µmol/L (Control, ZEA10, ZEA20, ZEA40) for 24 and 36 h. The Keap1 (A), Nrf2 (B), Nqo1 (C), and Ho1 (D) mRNA relative expression of IPEC-J2 cells. a–d The mean values differ significantly (p < 0.05).
Fig 5: Schematic diagram of the mechanism by which miR-181d affects OC chemoresistance via the OGT/KEAP1/NRF2 axis.miR-181d directly targets OGT and inhibits the expression of OGT, thereby inhibiting the glycosylation of KEAP1, reducing the ubiquitination, and degradation of NRF2 and promoting the expression of NRF2. By this mechanism, the viability of OC cells is promoted while cell apoptosis is suppressed, ultimately inducing the chemoresistance of OC.
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