Figure 2.

Interaction between nuclear factor erythroid 2 (Nrf2) and nuclear factor kappa B (NF-κB) in the modulation of the oxidative stress and inflammation Legend: Molecular mechanisms involved in the inflammatory and antioxidant response in intestinal epithelial cells, following recognition of bacterial LPS (lipopolysaccharide) by TLR4 (Toll-like receptor 4). TLR4 activation triggers two main pathways: (1) The Nrf2 pathway (nuclear factor erythroid 2-related factor 2), with the activation of the transcription of antioxidant genes, such as HO-1 (heme oxygenase-1), GCLC (glutamate-cysteine ligase catalase), CAT (catalase), and SOD (superoxide dismutase), which combat oxidative stress induced by reactive oxygen species (^•OH, H₂O₂, and NO^•). (2) NF-κB (nuclear factor kappa B) pathway: activation of the transcription of pro-inflammatory genes, including cytokines (IL-1β, IL-6, and TNF-α), chemokines (IP-10, MCP-1, and MIP-1), and enzymes (COX-2 and iNOS), which amplify the inflammatory response. The figure illustrates the complex interaction between the Nrf2 and NF-κB signaling pathways, which modulate the cellular response to oxidative stress and inflammation in the intestinal epithelium. The balance between these pathways is crucial for maintaining intestinal homeostasis and preventing tissue damage.