To investigate the relationship between RHO/ROCK signal pathway, neuroinflammatory reaction and pathological injury in rat brain after traumatic brain injury (TBI).

Forty-five healthy SD rats were randomly divided into control group, trauma group and intervention group with 15 rats in each group. The brain injury model of rats was made by using the principle of free fall of hammer and impact bar, and the intervention group model was made by injecting RHO/ROCK signal pathway blocker into the tail vein of brain injury rats. The rats in each group were sacrificed 24 h after TBI, and the contents of ROCKⅡ and nuclear transcription factor-κB (NF-κB) in the brain tissue of the rats in each group were observed by immunohistochemistry and determine its gray value; The ultrastructural changes of brain cells in the injured area of rats in each group were observed by electron microscope.

There was statistically significant difference in the content of ROCK Ⅱprotein in the brain of rats in the three groups 24 h after TBI (F=28.990, 68.454, P<0.001). The content of ROCK Ⅱprotein in the trauma group was the highest, the intervention group was the middle, and the control group was the lowest, the difference was statistically significant (P<0.05). Through electron microscope bservation, it was found that the damaged area of brain tissue in rats after TBI showed severe nuclear deformation, shrinkage and irregularity, dispersed nucleoli, increased chromatin content, increased synaptic vesicles, scattered mitochondria, edema, disappearance of mitochondrial cristae, and serious edema of nerve cells. In the intervention group, the nuclei were irregular in the damage area; no increased chromatin, more synaptic vesicles, mitochondrial edema, mitochondrial edema, tissue edema was less than that in the trauma group.

The content of ROCKⅡ and NF-κB can be reduced by blocking the RHO/ROCK signaling pathway, and the degree of inflammation and pathological damage in the brain of mice can be reduced after TBI.