Zi-Ran Wang1, Yu-Xin Li1, Hong-Yan Lei1, Dai-Qun Yang1, Li-Quan Wang1, Ming-Yu Luo2. 1. Department of Cerebral Surgery, Linyi People's Hospital, Shandong 276000, China. 2. Department of Cerebral Surgery, Linyi People's Hospital, Shandong 276000, China. Electronic address: nyjzlhy@163.com.
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.
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.
Authors: William T O'Brien; Louise Pham; Georgia F Symons; Mastura Monif; Sandy R Shultz; Stuart J McDonald Journal: J Neuroinflammation Date: 2020-04-06 Impact factor: 8.322
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