TLR4 and serum lipopolysaccharide activity: Therefore, we hypothesized that endotoxemia induced impairment of 5-HT neuron transmitter metabolism and activation of neuron immune cells are involved in the pathophysiologic process of endotoxemia induced acute neuro-inflammation and cognitive impairement16, and dioscin ameliorates endotoxemia induced acute neuro-inflammation and accommodates neuron inflammation through HMGB-1/TLR4 signaling pathway.