041 Biogenic nano-selenium particles effectively attenuate oxidative stress–induced intestinal epithelial barrier injury by activating the Nrf2 antioxidant pathway

Abstract

Supplemental Figure S1. Toxicity of diquat in mice. Thirty mice (five-week-old) were chosen to establish the mouse model of intestinal oxidative stress. After one week of adaption, these mice were randomly allocated into six groups (n=5) and treated as follows: (a) PBS (control group), (b) 12 mg/kg diquat group, (c) 25 mg/kg diquat group, (d) 50 mg/kg diquat group, (e) 75 mg/kg diquat group, (f) 100 mg/kg diquat group. Equal volumes of diquat or PBS was injected intraperitoneally. Twelve hours after treatment, the mice that survived were counted and samples of their blood, liver, duodenum, jejunum, ileum and colon were collected.

Selenium-Enriched Pediococcus acidilactici MRS-7 Alleviates Patulin-Induced Jejunum Injuries in Mice and Its Possible Mechanisms

“…This is similar to previous reports that compared to adequate Se supplementation, high doses of Se administration (0.4 mg/kg in the diet) were more effective in modulating the inflammation-related cytokines in mice. ,, The cellular antioxidant transcription factor Nrf2 could also regulate the expression of various antioxidant genes to eliminate excessive ROS produced by mitochondria. , In this research, the Nrf2 mRNA expression level significantly decreased after PAT exposure ( p < 0.001), while 0.15-SeP and 0.40-SeP could significantly alleviate this alteration ( p < 0.001) (Figure C). Similarly, Song et al reported that Se protected the intestinal barrier by activating Nrf2 and its downstream genes . The western blot results showed that compared with the control group, the protein expression level of antioxidant transcription factor Nrf2 was significantly decreased, the protein levels of proinflammatory factors NF-κB and TLR-4 were significantly increased after the PAT treatment (Figure A–C), while 0.15-SeP and 0.40-SeP increased the Nrf2 protein level and inhibited NF-κB and TLR-4 protein levels ( p < 0.001), thus regulating PAT-induced inflammation and oxidative stress in mice.…”

“…Similarly, Song et al reported that Se protected the intestinal barrier by activating Nrf2 and its downstream genes. 50 The western blot results showed that compared with the control group, the protein expression level of antioxidant transcription factor Nrf2 was significantly decreased, the protein levels of proinflammatory factors NF-κB and TLR-4 were significantly increased after the PAT treatment (Figure 3A protein levels' the protein level of NF-κB was higher than that of the PAT group. 3.6.…”

Anti-inflammatory and Antioxidative Effects of Tetrahedral DNA Nanostructures via the Modulation of Macrophage Responses

“…Oxidative stress refers to the production of intracellular ROS and antioxidant imbalance. 48 It leads to protein modification, lipid peroxidation, and subsequent cellular dysfunction 49 via the production of free radicals and is an important factor in aging and disease progression. To investigate whether TDNs play a role in antioxidative action, a fluorescence assay was developed by incorporating a DCFH-DA fluorescent probe into cells.…”

Thioredoxin reductase 3 suppression promotes colitis and carcinogenesis via activating pyroptosis and necrosis

“…Txnrd family as selenoproteins are involved in several colon diseases. Recently, Song et al found that increase of Txnrd1 effectively attenuate oxidative stress induced injury of intestinal epithelial barrier (22). However, another research indicated that there is no effect in TXNRDs activity during Se deprivation but GPX1 and SelP differentially decreased in contrast (23).…”