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 κB (NF‐κB)‐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‐κB, lessen concentrations of tumour necrosis factor α, interleukin‐1β 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 concentration–response relationship was not found. Thus, GB may inhibit TLR‐4 and NF‐κB‐dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI, which may support the use of GB for the treatment of TBI. Copyright © 2012 John Wiley & Sons, Ltd.