摘要
Background Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances （including water） into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury.Methods In part one, methylene blue was injected into the rabbits’ cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor （TNF）-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 （IL-1）, IL-10, interferon （IFN）-γ, transforming growth factor （TGF）-β, anti-brain antibodies （ABAb）, and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H＆E staining. Results In part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group （P 〈0.05）. Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid （CSF） injected group were higher than in the control cerebrospinal fluid injected group （P 〈0.05）. In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate （Glu）, neuronal degeneration and number of peripheral blood leukocytes were lower in the group wit
Background Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances （including water） into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury.Methods In part one, methylene blue was injected into the rabbits’ cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor （TNF）-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 （IL-1）, IL-10, interferon （IFN）-γ, transforming growth factor （TGF）-β, anti-brain antibodies （ABAb）, and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H＆E staining. Results In part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group （P 〈0.05）. Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid （CSF） injected group were higher than in the control cerebrospinal fluid injected group （P 〈0.05）. In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate （Glu）, neuronal degeneration and number of peripheral blood leukocytes were lower in the group wit
