Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury

Objective To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-kappa B)-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-kappa B, concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1 beta) 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-kappa B, lessen concentrations of TNF-alpha, IL-1 beta 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-kappa B-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.