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   <subfield code="a">Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Xiao-Qiao Dong, Wen-Hua Yu, Yue-Yu Hu, Zu-Yong Zhang, Man Huang]</subfield>
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   <subfield code="a">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 120mg/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 120mg/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&lt;0.05), but the administration of 60mg/kg OMT could not (P&gt;0.05). Conclusion: OMT may inhibit TLR4/NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.</subfield>
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   <subfield code="u">Department of Neurosurgery, The First Hangzhou Municipal People's Hospital, Nanjing Medical University, 261 Huansha Road, 310000, Hangzhou, China</subfield>
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   <subfield code="u">Department of Neurosurgery, The First Hangzhou Municipal People's Hospital, Nanjing Medical University, 261 Huansha Road, 310000, Hangzhou, China</subfield>
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