Hyperbaric oxygen therapy (HBOT) has shown potential in treating inflammatory bowel disease (IBD). IBD, characterized by chronic inflammation in the gastrointestinal tract, is associated with increased oxidative stress, mucosal inflammation, and microbial dysbiosis. HBOT, which involves breathing pure oxygen at higher-than-normal atmospheric pressure, has been shown to reduce oxidative stress, inhibit mucosal inflammation, promote ulcer healing, and influence gut microbes. It may also reduce the incidence of IBD complications by modulating inflammatory responses and enhancing antioxidant activity. HBOT reduces oxidative stress by increasing the levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), thereby decreasing oxidative stress markers like malondialdehyde (MDA). This reduction in oxidative stress helps alleviate tissue damage and supports the healing of intestinal ulcers. Additionally, HBOT has been shown to reduce the levels of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS), while increasing the levels of anti-inflammatory cytokines like interleukin-10 (IL-10). This dual effect on cytokines helps mitigate the inflammatory response and reduce tissue damage. HBOT also promotes the healing of the intestinal epithelial barrier by upregulating the production of mucin (MUC2), which is essential for maintaining the integrity of the intestinal lining. It enhances stem cell differentiation and recruitment of repair cells, which contributes to the repair of the intestinal epithelial barrier. Furthermore, HBOT improves blood supply to wounds by promoting angiogenesis, which is crucial for tissue repair and healing. HBOT has been shown to affect gut microbes by altering the composition of the intestinal flora, which may contribute to the therapeutic effects in IBD. It has also been effective in treating various IBD-related complications, including perianal fistulas, enterocutaneous fistulas, and pyoderma gangrenosum. Clinical studies have demonstrated that HBOT can lead to significant improvements in symptoms and outcomes for patients with IBD. Despite these promising findings, further research is needed to fully understand the mechanisms of HBOT in IBD and to establish standardized treatment protocols. The safety and effectiveness of HBOT in treating IBD require further investigation, and more large-scale clinical trials are necessary to validate its therapeutic potential. Overall, HBOT shows promise as a complementary therapy for IBD, offering a potential avenue for improving patient outcomes and quality of life.Hyperbaric oxygen therapy (HBOT) has shown potential in treating inflammatory bowel disease (IBD). IBD, characterized by chronic inflammation in the gastrointestinal tract, is associated with increased oxidative stress, mucosal inflammation, and microbial dysbiosis. HBOT, which involves breathing pure oxygen at higher-than-normal atmospheric pressure, has been shown to reduce oxidative stress, inhibit mucosal inflammation, promote ulcer healing, and influence gut microbes. It may also reduce the incidence of IBD complications by modulating inflammatory responses and enhancing antioxidant activity. HBOT reduces oxidative stress by increasing the levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), thereby decreasing oxidative stress markers like malondialdehyde (MDA). This reduction in oxidative stress helps alleviate tissue damage and supports the healing of intestinal ulcers. Additionally, HBOT has been shown to reduce the levels of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS), while increasing the levels of anti-inflammatory cytokines like interleukin-10 (IL-10). This dual effect on cytokines helps mitigate the inflammatory response and reduce tissue damage. HBOT also promotes the healing of the intestinal epithelial barrier by upregulating the production of mucin (MUC2), which is essential for maintaining the integrity of the intestinal lining. It enhances stem cell differentiation and recruitment of repair cells, which contributes to the repair of the intestinal epithelial barrier. Furthermore, HBOT improves blood supply to wounds by promoting angiogenesis, which is crucial for tissue repair and healing. HBOT has been shown to affect gut microbes by altering the composition of the intestinal flora, which may contribute to the therapeutic effects in IBD. It has also been effective in treating various IBD-related complications, including perianal fistulas, enterocutaneous fistulas, and pyoderma gangrenosum. Clinical studies have demonstrated that HBOT can lead to significant improvements in symptoms and outcomes for patients with IBD. Despite these promising findings, further research is needed to fully understand the mechanisms of HBOT in IBD and to establish standardized treatment protocols. The safety and effectiveness of HBOT in treating IBD require further investigation, and more large-scale clinical trials are necessary to validate its therapeutic potential. Overall, HBOT shows promise as a complementary therapy for IBD, offering a potential avenue for improving patient outcomes and quality of life.