Neuroinflammation in the brain is the response of central nervous system immune cells and peripheral immune systems when the brain experiences trauma, injury, or other pathological conditions. It is mainly produced by microglia and astrocytes, or infiltrates peripheral immune system cells when the blood-brain barrier is compromised, and these cells secrete various pro-inflammatory cytokines. While neuroinflammation is a necessary process for tissue repair, a chronically overactive state of the immune system, often referred to as chronic inflammation, can lead to widespread tissue damage such as AD, autism, CP, and TBI.
One of the neurodegenerative diseases highly associated with neuroinflammation is AD. In AD, massive amyloid plaques build up in the brain. These plaques may lead to microgliosis, in which activated microglia surround the plaque and secrete pro-inflammatory cytokines. Shapira et al. studied the effect of hyperbaric oxygen treatment on a mouse model of AD and found that microglia around amyloid plaques were reduced after treatment, as well as pro-inflammatory cytokines such as TNF-α, as demonstrated by immunofluorescent staining of the hippocampus. Show. These researchers believe that the reduction in the number of cytokines may be due to the reduction in the number of microglia. In addition, morphological examination revealed that hyperbaric oxygen treatment enhanced the extension of microglial processes and increased the number of microglia sprouting around plaques, which may indicate changes in microglial activation status and function. These findings were accompanied by reductions in hypoxia levels and the number of amyloid plaques, as well as improvements in cognition and anxiety-related behaviors.
Several studies have found that, in addition to reducing the secretion of pro-inflammatory cytokines, hyperbaric oxygen treatment reduces neuroinflammation by enhancing the secretion of anti-inflammatory cytokines by immune cells. In animal models, hyperbaric oxygen treatment increased expression levels of mRNA encoding the anti-inflammatory cytokine interleukin (IL-4), as measured by real-time quantitative PCR, and increased concentrations of the anti-inflammatory cytokine IL-10. Cortex measured by ELISA. Changes in anti-inflammatory cytokines have also been found in human patients with various neurological disorders.
The anti-inflammatory effect of hyperbaric oxygen treatment can promote tissue repair and prevent secondary cell death by blocking the apoptotic pathway. This was demonstrated in a mouse model of TBI, in which increased expression of the anti-inflammatory cytokine IL-10 after hyperbaric oxygen treatment resulted in decreased caspase-3 activity and concomitantly reduced Bax expression levels. To sum up, these findings suggest that hyperbaric oxygen treatment not only prevents future damage but also initiates the healing process in tissues.