|
Model | The effect of activating Nrf2 | Reference |
|
S. typhimurium infection | Oxidative stress and colitis decreased. | Theiss et al. [11] |
Dextran sodium sulfate-induced colitis model | Numbers of aberrant crypt foci decreased, and colonic proinflammatory cytokine, myeloperoxidase activity, 3-nitrotyrosine immunoreactivity, and lipid peroxidation decreased. Aconitase activity increased. | Osburn et al. [12] |
Burn-injured model | Damage of gut structure, intestinal permeability, and inflammatory cytokines (IL-6, IL-1β, MCP-1, intercellular adhesion molecule, and vascular cell adhesion molecule) decreased. NAD(P)H dehydrogenasequinine-1 and glutamate-cysteine ligase modifier subunit increased. | Chen et al. [17] |
Intestinal ischemia reperfusion injury model | Mucosal 15-F2t-isoprostane was reduced. Endogenous antioxidant superoxide dismutase activity was elevated. | Han et al. [14] |
Rat liver transplantation model | HO-1 expression was elevated. Tight junction function was restored. | Chi et al. [15] |
Traumatic brain injury model | Apoptosis-mediated intestinal epithelial cell damage was diminished. Intestinal permeability was improved. | Liu et al. [19] |
Aspirin/NSAID-induced vascular damage model | NSAID-induced vascular permeability was reduced. Mucosal MPO activity increased. Anaerobic enterobacterial count decreased. | Yanaka et al. [16] |
Severe sepsis model | Injuries caused by oxidative stress and inflammation were alleviated. HMGB1 levels was reduced, but HO-1 levels increased. | Yu et al. [18] |
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