Ginkgolide B Reduces Neuronal Cell Apoptosis in the Traumatic Rat Brain: Possible Involvement of Toll-like Receptor 4 and Nuclear Factor Kappa B Pathway

Ginkgolide B (GB) has been demonstrated to have a variety of pharmacological actions. Accumulating evidence indicates that GB may exert a protective effect on brain injury. The study was designed to investigate the influence of GB on toll-like receptor 4 (TLR-4) and nuclear factor kappa B (NF-kappa B)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI). Wistar rats were subjected to 5, 10 and 20 mg/kg GB daily for 5 days, intraperitoneally, following TBI. Rats were sacrificed at hour 2, 6 and 12, as well as day 1, 2, 3 and 5 after TBI. The administration of 10 and 20 mg/kg GB could significantly (least-significant difference test: p<0.05) suppress gene expressions of TLR-4 and NF-kappa B, lessen concentrations of tumour necrosis factor a, interleukin-1 beta and interleukin-6, as well as reduce the number of apoptotic neuronal cells in traumatic rat brain tissues, but the administration of 5 mg/kg GB did not (p>0.05). However, a clear concentrationresponse relationship was not found. Thus, GB may inhibit TLR-4 and NF-kappa B-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI, which may support the use of GB for the treatment of TBI. Copyright (c) 2012 John Wiley & Sons, Ltd.