Hyperbaric Oxygen Preconditioning Induce The Changes Of Microglia Phenotypes In Intracerebral Hemorrhage

BackgroundTo neurosurgery,high blood pressure,post-traumatic delayed cerebral hemorrhage,cerebral vascular disease are risk factors of intracerebral hemorrhage(ICH);Intracranial surgery must be accompanied by more or less ICH.Brain hematoma and brain edema by inflammation and hemorrhage after brain tissue compression injury,ischemia,hypoxia,cytotoxic effects of environmental changes in brain tissue and the decisive factor.Brain edema damage may lead to low brain activity,the change of cerebral blood flow and brain tissue metabolism,relieve cerebral edema can also be controlled to reduce after brain injury of nerve function defect,Microglia as settled within the brain tissue of mononuclear cell line scavenger primary immune cells,mainly in the brain inflammation plays a and take part in the inflammatory response and the role of nerve repair,M1 microglia can release inflammatory reaction medium,involved in the process of secondary injury after brain hemorrhage,cause nerve function defect and neuronal cell death;And M2 type of microglia can delay cell damage effect by cutting inflammation factor or by removal of necrotic tissue and actively participate in nerve regeneration.Hyperbaric oxygen therapy can relieve edema and improve brain ischemia hypoxia,improve tissue oxygen partial pressure and oxygen content,increase oxygen supply to the tissue damage,can relieve inflammation of the central nervous system,is advantageous to the nerve recovery of injured area and reduce bleeding in the intracerebral hemorrhage and ischemia secondary damage of brain tissue.On this basis,we put forward the HBOP treatment can induced microglia phenotypic changes in cerebral hemorrhage after nerve protective effect hypothesis,The research is divided into three parts: The first part are of HBOP on experimental rat model and autologous blood into the cerebral hemorrhage model in rats.At the second part of this studies,we research HBOP affect nerve inflammation and neuroprotection.At the third part we explore the protection mechanism of HBOP.Part ? the research of hyperbaric oxygen preconditioning(HBOP)in the acute phase of cerebral hemorrhageObjectiveClear HBOP in the acute phase of cerebral hemorrhage,to explore HBOP in inflammatory reaction and neural functional recovery mechanisms play a role.Methods1.Establish SD rats of autologous blood injection and HBOP in treatment of intracerebral hemorrhage(ICH)model.2.The experimental SD rats were randomly divided into sham group,ICH group and HBOP group,each group of 27 only the experimental rats3.The SD rats of autologous blood injection after ICH model building,stability of head mri scans detection model4.Evaluate the behavior score after the surgery,HBOP effect on neural functional recovery.5.Brain water content is determined by the dry-wet weight method,understand the degree of the inflammatory response in the HBOP group6.Use the Fluoro-Jade C neural degeneration degree between the different groups,to observe the effects of HBOP on neural decline7.Application of immunofluorescence labeling method and western blot analysis the expression of TNF alpha inflammatory markers detection,the effects of HBOP in response to inflammationResults1.HBOP in treatment of 72 h after cerebral hemorrhage showed obvious improvement of behavior,but in 12 h,24 h did not show obvious advantage.2.HBOP group in 12 h,24 h,72 h the three time points brain water content reduce obviously.3.HBOP in the organization of neural degeneration was significantly reduced,the decline and fall dramatically reduce the number of nerve cells.4.After HBOP,inflammation within the brain tissue factor expression of TNF alpha relative to the ICH group showed a statistically significant decrease.ConclusionHBOP can improve motor function in the acute phase of ICH is obvious,and can effectively reduce brain tissue water content at early phase after ICH,the early inflammatory response after ICH by HBOP treatment was significantly reduced.At the same time,neural degeneration after ICH,illustrates the HBOP can play a role in the neuroprotection after ICH.Through the study of the determination of TNF alpha inflammatory markers,we found HBOP could effectively reduce the expression of TNF alpha after ICH.Inflammatory markers M1 microglia and TNF alpha were positively correlated,that HBOP could induce the microglial phenotypic changes after ICH.Part ? HBOP changes microglia phenotypic in ICHObjectiveHBOP in the acute period of ICH on the impact of microglia,and explore the small plastic cell M1 and M2 in the process of dynamic change.Methods1.By immunofluorescence labeling and immunoblot analysis detection the expression of microglia markers Iba-1,observe the HBOP affects the quantity of microglia expression2.By immunofluorescence double label and immunoblot assay microglia markers and M1 Iba-1 type of small rubber cell markers CD11 b ratio change,explore the microglia M1 / M2 phenotypes in the process of dynamic changeResults1.HBOP treatment in 12 h,24 h,72 h after the three time points were found to have relative to the group of the reduction in the number of microglia intracerebral hemorrhage.2.HBOP treatment can change the positive expression rate of CD11 b and Iba-1,HBOP group CD11b/Iba-1 ratio decreased significantlyConclusionIn the acute phase after hemorrhage rats,HBOP group can effectively reduce the microglia activation to reduce brain secondary injury in the acute phase of inflammation reaction process.At the same time,HBOP can reduce microglial markers CD11 b proportion of microglia M1,it also suggests that the M2 phenotype relatively increase in the proportion of microglia.M2 type to reduce inflammation,reduce nerve degeneration,and promote the role of nerve repair.Through reducing microglia inflammatory injury related proportion of M1 phenotype,increasing the M2 phenotypre percentage to play neuro-protective effect.