Anti-Inflammatory Effects of Hyperbaric Oxygenation during DSS-Induced Colitis in BALB/c Mice Include Changes in Gene Expression of HIF-1α, Proinflammatory Cytokines, and Antioxidative Enzymes

Figure 7

Proposed mechanisms mediating effects of HBO₂ on the inflammation during DSS-induced colitis. Compared to untreated DSS-induced colitis (left of the vertical dotted line), high partial pressure of oxygen during HBO₂ (right) activates HIF-1α signaling which leads to higher CAT and GPx1 mRNA expression resulting in reduced oxidative stress in the inflamed colonic mucosa. HIF-1α mediated (negative) transcriptional regulation of proinflammatory cytokine IL-6 and reduced oxidative tissue injury leads to decreased neutrophil, monocyte, and lymphocyte adhesion and infiltration to the gut mucosa. In addition, HBO₂ activates genes encoding for barrier-protection and genes responsible for improving tight junction integrity, all together resulting in reduced number of bacteria entering the lamina propria of gut mucosa. T ly, T lymphocyte; B ly, B lymphocyte; DC, dendritic cell; Ne, neutrophil; Mo, monocyte/macrophage; HIF-1α, hypoxia inducible factor 1 alpha; CAT, catalase; GPx1, glutathione peroxidase 1; SOD1, superoxide dismutase 1; pO₂, partial O₂ pressure; ↑, increased; ↓, decreased.