Neuroprotective Effects of Pretreatment with Propofol in LPS-Induced BV-2 Microglia Cells: Role of TLR4 and GSK-3β: Role of TLR4 and GSK-3β

Surgery often leads to neuroinflammation, which mainly acts as the activation of microglia cells. Propofol is always used for induction and maintenance of anesthesia prior to surgical trauma, whereas whether or not it could attenuate neuroinflammation used prophylactically is not well defined. In the present study, we incubated BV-2 microglia cells with 1 μg/ml lipopolysaccharide (LPS) to mimic neuroinflammation in vitro . Firstly, cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and the data indicated that propofol would not reduce cell viability unless its concentration reached 300 μM. Secondly, BV-2 microglia cells were pretreated with 30 μM propofol (clinically relevant concentration), and then stimulated with LPS. The results showed that the production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-10 was considerably increased by LPS, but the change could be markedly attenuated by pretreatment with propofol. Meanwhile, pretreatment with propofol inhibited LPS-induced augmentation of toll-like receptor 4 (TLR4) expression at both mRNA and protein levels and further upregulated LPS-induced inactivation of glycogen synthase kinase-3β (GSK-3β) in BV-2 microglia cells. These results indicated, at least in part, that pretreatment with propofol can protect BV-2 microglia cells against LPS-induced inflammation. Downregulation of TLR4 expression and inactivation of GSK-3β may be involved in its protective effect.