Ketamine attenuates the lipopolysaccharide-induced inflammatory response in cultured N2a cells

The use of ketamine is recommended in patients with sepsis undergoing surgery due to its anti-inflammatory effects. However, a paucity of data exists with regard to the anti-inflammatory effects of ketamine in the central nervous system. Therefore, the present study aimed to investigate the effect of ketamine on lipopolysaccharide (LPS)-induced inflammatory responses in cultured Neuro2a (N2a) cells and to elucidate its potential mechanism of action. N2a cells were randomly divided into the following 3 groups (n=6): The DMEM culture solution administration alone group, the 0.5 mu mol/l LPS administration alone group and the 1 mu mol/l ketamine plus 0.5 mu mol/l LPS administration group. The expression levels of interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, nuclear factor (NF)-kappa B and inducible nitric oxide synthase (iNOS) were determined. LPS-treated N2a cells exhibited a significant increase in the expression levels of IL-1 beta, IL-6, TNF-alpha, NP-kappa B and iNOS, while the administration of ketamine eliminated the LPS-induced, production of IL-1 beta, IL-6, TNF-alpha, NF-kappa B and iNOS. Based on our data, we hypothesized that the anti-inflammatory effect exerted by ketamine on N2a cells was potentially due to the inhibition of NF-kappa B and iNOS.