Hyperbaric oxygen preconditioning attenuates neuroinflammation after intracerebral hemorrhage in rats by regulating microglia characteristics.

Intracerebral Hemorrhage (ICH) results in a detrimental neurologic disorder with complicated secondary brain injury. Hyperbaric oxygen preconditioning (HBOP) may be a safe and effective therapeutic method for ICH victims. Our previous studies have demonstrated that HBOP induces neuroprotection in cerebral ischemia and traumatic brain injury. This study aimed to investigate whether HBOP could alleviate neuroinflammation by regulating changes in microglia characteristics in a rat model of ICH. ICH was induced by autologous arterial blood injection, and animals were sacrificed at 12, 24, and 72 h post injury. We measured motor function and brain water content to evaluate the extent of inflammation. Fluoro-Jade C and TNF-α staining was used to characterize neuronal degeneration and neuroinflammatory cytokines, and immunofluorescence staining was performed for CD11b to show activated microglia and Iba-1 to show microglia. Our results indicate that motor dysfunction and brain water content are alleviated by HBOP, and Fluoro-Jade C staining demonstrates that neuron degeneration decreased in the HBOP group. The growth of Iba-1-positive microglia decreased in the HBOP group. Moreover, TNF-α was dynamically reduced in the HBOP group compared with the ICH group. CD11b-Iba-1 double staining demonstrated that the ratio of CD11b and Iba-1 was significantly decreased in the HBOP group. Overall, the data demonstrated that HBOP could significantly alleviate the ICH-induced neuroinflammation by regulating microglia characteristics changing. The phenomenon may propel the progress of the relation between microglia and HBOP and represent a novel target for ICH treatment.