Hyperbaric oxygen therapy reduces the traumatic brain injury-mediated neuroinflammation through enrichment of Prevotella copri in the gut of male rats

Abstract

Abstract Background Gastrointestinal dysfunction frequently occurs following traumatic brain injury (TBI) and significantly increases posttraumatic complications. TBI can lead to alterations of gut microbiota. The neuroprotective effects of hyperbaric oxygen (HBO) have not been well recognized after TBI. The study aim was to link the impacts of HBO on the TBI-induced dysbiosis in the gut and the pathological changes in the brain after TBI. Material and method : Anesthetized male Sprague–Dawley rats were randomly assigned to 3 groups: sham surgery plus normobaric air (NBA) (21% oxygen at 1 ATA), TBI (2.0 atm) plus NBA, and TBI (2.0 atm) plus HBO (100% oxygen at 2.0 ATA) for 60 minutes immediately after TBI, 24 hours, and 48 hours later. The brain injury volume, TNF-α expression in the microglia and astrocyte, and neuronal apoptosis in the brain were consequently determined. The V3/V4 regions of 16S rRNA of the fecal samples were sequenced, and alterations of the gut microbiome were statistically analyzed. All parameters were evaluated at the 3rd day after TBI. Results Our results showed HBO improved TBI-induced neuroinflammation, brain injury volume and neuronal apoptosis. HBO appeared to increase the abundance of aerobic bacteria but inhibit anaerobic bacteria. Intriguingly, HBO reversed the TBI-mediated decrease of Prevotella copri and Deinococcus spp., which were both negatively correlated with neuroinflammation and brain injury volume. TBI increased the abundance of these gut bacteria in relation to NOD-like receptor signaling and Proteasome pathway, which also had a positive correlation trend to neuroinflammation and apoptosis. The abundance of Prevotella copri was negatively correlated to NOD-like receptor signaling and Proteasome pathway. Conclusion Our study demonstrated the neuroprotective effects of HBO after acute TBI might act through reshaping the TBI-induced gut dysbiosis and reversed the TBI-mediated decrease of Prevotella copri to reduce TBI-induced neuroinflammation through inhibition NOD-like receptor signaling and Proteasome pathway.