Hyperbaric oxygen preconditioning attenuates brain injury after intracerebral hemorrhage by regulating microglia polarization in rats.

Abstract

AimsHyperbaric oxygen preconditioning (HBOP) attenuates brain edema, microglia activation, and inflammation after intracerebral hemorrhage (ICH). In this present study, we investigated the role of HBOP in ICH‐induced microglia polarization and the potential involved signal pathway.MethodsMale Sprague‐Dawley rats were divided into three groups: SHAM, ICH, and ICH + HBOP group. Before surgery, rats in SHAM and HBOP groups received HBO for 5 days. Rats in SHAM group received needle injection, while rats in ICH and ICH + HBOP groups received 100 μL autologous blood injection into the right basal ganglia. Rats were euthanized at 24 hours after ICH, and the brains were removed for immunohistochemistry and Western blotting. Neurological deficits and brain water content were determined.ResultsIntracerebral hemorrhage induced brain edema, which was significantly lower in the HBOP group. The levels of MMP9 were also less in the HBOP group. HBO pretreatment resulted in less neuronal death and neurological deficits after ICH. Their immunoactivity and protein levels of M1 markers were downregulated, but the M2 markers were unchanged by HBOP. In addition, ICH‐induced pro‐inflammatory cytokine (TNF‐α and IL‐1β) levels and the phosphorylation of JNK and STAT1 were also lower in the HBOP rats.ConclusionsHBO pretreatment attenuated ICH‐induced brain injuries and MMP9 upregulation, which may through the inhibiting of M1 polarization of microglia and inflammatory signal pathways after ICH.