Abstract
Ginkgolide B (GB) is widely used in the treatment of neurological diseases and exerts anti-inflammatory and neuroprotective effects. Microglia serve an important role in central nervous inflammation. The present study investigated the effect of GB on central nervous inflammation in vivo and in vitro. BV2 cells were activated with lipopolysaccharide (LPS) to establish a cellular model of neuroinflammation. Cell viability was determined using the Cell Counting Kit-8 assay and the secreted levels of TNF-α, IL-1 and IL-6 were measured using ELISAs. The levels of nitric oxide (NO) was assessed using Griess assays. In addition, the mRNA and protein expression levels of inducible NO synthase and cyclooxygenase-2 (COX-2) were detected using reverse transcription-quantitative PCR and western blot analyses, respectively. Transwell assays were carried out to evaluate the cell migratory ability. For the in vivo studies, an LPS-induced neuroinflammation model was established in C57 mice. Western blot analysis and immunohistochemistry were performed to detect the expression of the microglial marker allograft inflammatory factor 1 in the hippocampal dentate gyrus and striatum. The expression levels of TNF-α, IL-1 and IL-6 in the hippocampal dentate gyrus and striatum were assessed using western blot analysis. The results revealed that GB reduced the inflammatory response and migration of LPS-induced BV2 cells. Furthermore, GB attenuated the activation of BV2 cells of the hippocampal dentate gyrus and striatum in the LPS-induced mice with neuroinflammation. Taken together, the findings of the present study demonstrated that GB alleviated the inflammatory response and attenuated the activation of LPS-induced BV2 cells in vitro and in vivo.