The nuclear factor erythroid 2–related factor 2 (Nrf2) pathway is a central regulator of the cellular antioxidant response, playing a key role in modulating inflammation and defending against oxidative stress‐induced damage. A range of natural and synthetic compounds, including dimethyl fumarate, bardoxolone, oltipraz, RTA‐408, ursodiol, curcumin, sulforaphane, and resveratrol, have been shown to activate Nrf2 via distinct molecular mechanisms, thereby enhancing the expression of cytoprotective and antioxidant genes. These mechanisms include direct dissociation from Keap1, activation of AMP‐activated protein kinase, and modulation of signaling pathways relevant to cellular stress and immune regulation. In inflammatory diseases such as rheumatoid arthritis, periodontitis, diabetes mellitus, and inflammatory bowel diseases, Nrf2 activation has been associated with attenuation of oxidative damage, suppression of proinflammatory mediators, and improved tissue homeostasis. However, sustained or dysregulated activation of Nrf2 may promote tumor cell survival, proliferation, and chemoresistance, particularly in oncologic contexts. This narrative review synthesizes mechanistic insights and preclinical and clinical evidence on the role of Nrf2 in inflammatory diseases and evaluates the therapeutic potential of its key activators. The dual nature of Nrf2, as both a cytoprotective and potentially oncogenic factor, highlights the importance of context‐specific and temporally controlled modulation. A better understanding of these dynamics is essential for optimizing clinical applications and minimizing therapeutic risks.

[This retracts the article DOI: 10.1155/2019/2432416.].

[This corrects the article DOI: 10.1155/2022/2188145.].

Background: Premature activation of integrin α IIb β 3 plays a central role in the induction and development of the platelet storage lesion (PSL) characterized by an exhausted platelet phenotype that affects adhesion and spreading on fibrinogen. Given the role of reactive oxygen species (ROS) in regulating platelet activation per se, we investigated the effects of a ROS scavenger on reducing the functional decline of platelet integrin α IIb β 3 during storage. Methods: Platelet-rich plasma-platelet concentrates (PRP-PCs) were either treated with ROS-reducing agents (1 mM N-acetyl-L-cysteine [NAC] or 30 μM NADPH oxidase [NOX] inhibitor, VAS2870) or kept untreated during storage. CD41/CD61 (total integrin α IIb β 3) expression and PAC-1 binding (specific to active integrin α IIb β 3 conformation) were analyzed by flow cytometry over a 5 day storage period. Molecular changes in integrin β 3 subunit were evaluated by western blotting. Platelet adhesion/spreading to fibrinogen in the presence of ROS inhibitors was also investigated during storage using fluorescence microscopy. Results: A decrease in the molecular weight of integrin β 3 subunit was observed during platelet storage, and was significantly reduced by NAC but not VAS2870, suggesting proteolytic cleavage of β 3 during storage. Further to this, ROS inhibitors decreased integrin activation and increased platelet adhesion to fibrinogen from day 3 of storage, while NAC but not VAS2870 improved platelet spreading. Conclusion: This is the first report of increasing β 3 cleavage of integrin during storage that was inversely correlated with integrin α IIb β 3-mediated platelet function. In this regard, as a generic ROS scavenger, NAC was shown to reduce defects in platelet spreading through inhibition of β 3 cleavage. This is in contrast to VAS2870 which selectively inhibits cytosolic NOX alone, suggesting that the reduced platelet function observed during storage may be due to cumulative effects of mitochondrial ROS. Taken together, these studies suggest that adding NAC to platelets may significantly preserve optimal integrin α IIb β 3 and platelet function during storage. Moreover, as a reversible scavenger, its inhibitory effect can be readily compensated after transfusion.

This study intends to investigate the green synthesis of silver (Ag) and gold (Au) nanoparticles (NPs) using Echinophora platyloba extract and to evaluate the antioxidant and anti-inflammatory effects of the synthesized NPs and the extract. In this study, aqueous and hydroalcoholic extracts of E. platyloba were prepared, which were used for the biosynthesis of Ag and Au NPs. Dynamic light scattering (DLS), zeta potential analysis, transmission electron microscopy (TEM), Fourier transform infrared (FT-IR) spectroscopy, UV-Vis spectroscopy, and X-ray diffraction (XRD) methods were used to characterize the green NPs. The antioxidant effect of the NPs was estimated using in vitro methods, including reducing power (RP), ferric reducing/antioxidant power (FRAP), and 2,2-diphenyl-1-picrylhydrazyl (DPPH). To evaluate the anti-inflammatory and antioxidant activity of E. platyloba extract and Ag and Au NPs, we used the carrageenan method. In our experiment, the extract and the synthesized NPs were administered orally to the mice 2 h before the carrageenan injection. The subsequent inhibition of inflammation and reduction of paw thickness were quantified. To evaluate their antioxidant effect, malondialdehyde (MDA), and total antioxidant capacity (TAC) levels were measured. Levels of pro-inflammatory cytokines, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were also quantified. In this study, the results indicate that the synthesized Ag and Au NPs have antioxidant and anti-inflammatory effects. The most promising results were observed in the groups that received the Ag NPs.