The effect of hyperbaric oxygen therapy in the inflammatory response in a mouse model of endometriosis: An experimental study

Abstract

Background: Endometriosis pathogenesis is related to the inflammation shown by the secretion of pro-inflammatory mediators. This hypoxia condition can stimulate this condition.
 Objective: To investigate the effect of hyperbaric oxygen therapy (HBOT) on the inflammation reaction of endometriosis-induced mice.
 Materials and 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 (NFκB) beta was measured by immunohistochemical staining.
 Results: The results showed that group I demonstrated the highest level of inflammation degree (9.41 ± 1.99) compared to the post-test groups (group II: 1.60 ± 0.53; group III: 2.42 ± 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. NFκB expression on the post-test groups was significantly decreased, compared to the pre-test group (p ≤ 0.001), with a strong correlation between the NFκB expression and the peritoneal inflammation level (p ≤ 0.001, r = 0.670).
 Conclusion: HBOT significantly reduced the inflammation level on the endometrial lesion in mice, involving the NFκB pathway.
 Key words: Endometriosis, Hyperbaric oxygenation, Inflammation, Hypoxia, Mouse.

The Mechanisms of Action of Hyperbaric Oxygen in Restoring Host Homeostasis during Sepsis

“…Conversely, when HBO 2 treatment is administered in hypoxic conditions with a derivational elevated HIF-1α, HBO 2 treatment decreased the disease-mediated high levels of HIF-1α [ 61 , 119 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 ]. The evaluation of studies performed in conditions of relative hypoxia secondary to inflammation indicates that the effect of HBO 2 on HIF-1α protein expression is dependent on the number of HBO 2 sessions administered, with HBO 2 having an increasing effect when administered in up to five sessions [ 140 , 141 , 142 , 143 ], and treatment with more than six sessions having a decreasing effect under these conditions [ 47 , 120 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 ]. However, six study results were not supportive of this trend [ 117 , 140 , 141 , 157 , 158 , 159 ].…”

“…Studies looking at the impact of HBO 2 on the expression on NF-κB similarly found an increasing effect in a normoxic environment [ 17 , 117 , 160 ] and a decreasing effect in a hypoxic environment [ 161 , 162 ], regardless of the stage of inflammation. In contrast to HIF-1α expression, studies evaluating the effect on NF-κB signaling in conditions of relative hypoxia secondary to inflammatory conditions mostly found a decreasing effect regardless of the inflammatory state or number of HBO 2 sessions [ 46 , 47 , 153 , 154 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 ], with the exception of three studies where 10–30 sessions of HBO 2 were applied to chronic inflammation, which found an increasing effect [ 117 ] or no effect (Part b in Table 1 ) [ 149 , 158 ].…”