**3. Conclusions**

HBOT has been used as a primary or adjunctive therapy over the last 50 years, both in experimental and clinical studies. However, despite the decades of extensive research the entire spectrum of HBOT action is still not completely understood, although many mechanisms of its action have been proposed. Therefore, in this systematic review we elaborate the cellular and molecular mechanisms of HBOT actions. Based on the presented data it may be concluded that improved tissue oxygenation and cellular metabolism, anti-inflammation, anti-apoptosis, as well as intensifying of neuroplastic responses, promoting of synaptogenesis, neurogenesis and angiogenesis may constitute the multiple and complementary mechanisms underlying HBOT-induced neuroprotection. In addition, reduction of lipid peroxidation and up-regulation of antioxidant enzymes are among the mechanisms involved in the action of HBO. In that way, HBOT diminishes imbalance between oxidants and anti-oxidants that occurs after brain injury, and contributes to the maintenance of pro−/antioxidant homeostasis. Furthermore, HBOT effectively attenuates reactive astrogliosis and microgliosis, prevents tissue-damaging effects of neutrophils and suppresses formation of glial scar. Accordingly, by alleviating gliamediated inflammatory response and limiting production of inflammatory mediators HBOT fosters formation of more permissive environment for tissue repair, allowing the recovery of impaired brain functions. Overall, although results clearly suggest the validity of HBO therapy for the treatment of TBI, the underlying mechanism still needs to be studied in depth.
