ABSTRACT
Objective: To observe the effect of nuclear transcription factor-κB (NF-κB) on cerebral edema in rats with traumatic brain injury (TBI). Methods: Male SD rats with fluid percussion injury (FPI) were selected. After separation and culture, rats' astrocytes all suffered FPI. The expression of NF-κB and the water content were detected at the animal and cellular levels, while the activity of NOX was evaluated at the cellular level. Results: According to the results, the positive expression of NF-κB and expression of mRNA were significantly increased and the water content was increased for rats after TBI, while NF-κB inhibitor BAY11-7082 could significantly reduce the effect of TBI. 1 and 3 h after FPI of astrocytes, the activation of NF-κB was increased and BAY 11-7082 could significantly improve the injury-induced swelling of astrocytes. After the injury of astrocytes, the activity of NOX was also increased, while BAY 11-7082 could reduce the activity of NOX. Conclusions: The results show that the activation of NF-κB in astrocytes is a key factor in the process of cerebral edema after TBI of rats.
ABSTRACT
OBJECTIVE@#To observe the effect of nuclear transcription factor-κB (NF-κB) on cerebral edema in rats with traumatic brain injury (TBI).@*METHODS@#Male SD rats with fluid percussion injury (FPI) were selected. After separation and culture, rats' astrocytes all suffered FPI. The expression of NF-κB and the water content were detected at the animal and cellular levels, while the activity of NOX was evaluated at the cellular level.@*RESULTS@#According to the results, the positive expression of NF-κB and expression of mRNA were significantly increased and the water content was increased for rats after TBI, while NF-κB inhibitor BAY11-7082 could significantly reduce the effect of TBI. 1 and 3 h after FPI of astrocytes, the activation of NF-κB was increased and BAY 11-7082 could significantly improve the injury-induced swelling of astrocytes. After the injury of astrocytes, the activity of NOX was also increased, while BAY 11-7082 could reduce the activity of NOX.@*CONCLUSIONS@#The results show that the activation of NF-κB in astrocytes is a key factor in the process of cerebral edema after TBI of rats.