Xiao-Qiao Dong1, Wen-Hua Yu, Yue-Yu Hu, Zu-Yong Zhang, Man Huang. 1. Department of Neurosurgery, The First Hangzhou Municipal People's Hospital, Nanjing Medical University, 261 Huansha Road, Hangzhou, 310000, China. dxqhyy@163.com
Abstract
OBJECTIVE: To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI). MATERIALS AND METHODS: Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg OMT after TBI once a day till day 5. Rats were killed by decapitation at hours 2, 6 and 12, and days 1, 2, 3 and 5 after TBI. Gene expressions of TLR-4 and NF-κB, concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and interleukin-6 (IL-6) as well as the number of apoptotic neuronal cells in traumatic rat brain tissues were determined. RESULTS: The administration of 120 mg/kg OMT could significantly suppress gene expressions of TLR-4 and NF-κB, lessen concentrations of TNF-α, IL-1β and IL-6, and reduce the number of apoptotic neuronal cells in traumatic rat brain tissues by the Mann-Whitney U test (P < 0.05), but the administration of 60 mg/kg OMT could not (P > 0.05). CONCLUSION: OMT may inhibit TLR4/NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.
OBJECTIVE: To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI). MATERIALS AND METHODS:Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg OMT after TBI once a day till day 5. Rats were killed by decapitation at hours 2, 6 and 12, and days 1, 2, 3 and 5 after TBI. Gene expressions of TLR-4 and NF-κB, concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and interleukin-6 (IL-6) as well as the number of apoptotic neuronal cells in traumatic rat brain tissues were determined. RESULTS: The administration of 120 mg/kg OMT could significantly suppress gene expressions of TLR-4 and NF-κB, lessen concentrations of TNF-α, IL-1β and IL-6, and reduce the number of apoptotic neuronal cells in traumatic rat brain tissues by the Mann-Whitney U test (P < 0.05), but the administration of 60 mg/kg OMT could not (P > 0.05). CONCLUSION:OMT may inhibit TLR4/NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.