Regulating effect of activated NF-κB on edema induced by traumaticbrain injury of rats

• 作 者: Zi-Ran Wang Yu-Xin Li Hong-Yan Lei Dai-Qun Yang Li-Quan Wang Ming-Yu Luo
• 机 构: Department of Cerebral Surgery,Linyi People's Hospital,
• 出 处: Asian Pacific Journal of Tropical Medicine
• 发表日期: 2016年03期
• 关键词: Nuclear transcription factor-κB Traumatic brain injury Astrocytes Rat

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 rau with fluid percussion injury(FPI) were selected.After separation and culture,rats’ astrocytes all suffered FPL 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 BAY 11-7082 could significantly reduce the effect of TBI.1 and 3h after FPI of astrocytes,the activation of NFkB was incrcased 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 BAY11-7082 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.

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 rau with fluid percussion injury (FPI) were selected. After separation and culture, rats’ astrocytes all suffered FPL 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 BAY 11-7082 could significantly reduce the effect of TBI.1 and 3h after FPI of astrocytes, the activation of NFkB was incrcased 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 BAY11-7082 could reduce the activity of NOX. Conclusions: The results show that the activat ion of NF- κB in astrocytes is a key factor in the process of cerebral edema after TBI of rats.