Background
Endometriosis pathogenesis is related to the inflammation shown by the secretion of pro-inflammatory mediators. This hypoxia condition can stimulate this condition.
Conclusion
HBOT significantly reduced the inflammation level on the endometrial lesion in mice, involving the NF κκ<math><mi>κ</mi></math> B pathway.
Methods
The animals were designated into 3 groups: I) the pre-test group, II) the post-test group receiving the HBOT, and III) the post-test group without HBOT. All groups were subjected to induction of endometriosis by xenotransplantation for 15 days. HBOT was given 30 min 3 times a day for 10 days. The evaluation of the HBOT effect was conducted by examining the endometrial tissue. The inflammation level was evaluated using the Klopfleisch semiquantitative scoring system (index remmele scale), whilst the expression of nuclear factor kappa (NF κκ<math><mi>κ</mi></math> B) beta was measured by immunohistochemical staining.
Objective
To investigate the effect of hyperbaric oxygen therapy (HBOT) on the inflammation reaction of endometriosis-induced mice. Materials and
Results
The results showed that group I demonstrated the highest level of inflammation degree (9.41 ±±<math><mo>±</mo></math> 1.99) compared to the post-test groups (group II: 1.60 ±±<math><mo>±</mo></math> 0.53; group III: 2.42 ±±<math><mo>±</mo></math> 0.53). The HBOT-groups was found to have the lowest inflammation level compared to the non-HBOT group (p = 0.020). The results demonstrated that HBOT lowered the peritoneal inflammation degree caused by the endometrial lesion in mice. NF κκ<math><mi>κ</mi></math> B expression on the post-test groups was significantly decreased, compared to the pre-test group (p ≤≤<math><mo>≤</mo></math> 0.001), with a strong correlation between the NF κκ<math><mi>κ</mi></math> B expression and the peritoneal inflammation level (p ≤≤<math><mo>≤</mo></math> 0.001, r = 0.670).