The effect of different concentrations of sufentanil on interleukin-6 and tumor necrosis factor-α concentrations in peripheral blood induced by lipopolysaccharide

Abstract

Objective Investigating the effect of different concentration of sufentanil on IL-6 and TNF-α concentrations in human peripheral blood induced by lipopolysaccharide(LPS). Methods Every blood sample were collected from 30 healthy volunteers. Using a completely randomized design grouping method. Samples were randomized assigned in eight groups. Venous blood 5 ml from every volunteers were collected. 100 μl of the venous blood from every sample were put in eight ethylenediaminete-traacetic acid-vitro ready tubes labeled(A, B, C1, C2, C3, D1, D2, D3) by using precision pipette. Groups are: group A for the saline group(control), group B joined LPS 100 mg/L, group C includes C1, C2, C3, respectively fentanyl 0.05, 0.50, 5.00 μg/L, group D includes the D1, D2, D3 fentanyl 0.05, 0.50, 5.00 μg/L and LPS 100 mg/L, respectively. The IL-6 and TNF-α ELISA kit were used to detect supernatant concentrations of IL-6 and TNF-α. Results Group A and group C in peripheral blood IL-6 and TNF-α concentration were not significantly different(P>0.05). Plus LPS of group B and group D of IL-6, of TNF-α concentrations were significantly increased(P<0.05). Group D and group B, the peripheral blood of IL-6 and TNF-α concentrations were significantly lower(P<0.05). Group D2, D3 peripheral IL-6 and TNF-α concentration reduction are greater than the group D1(P<0.05). Group D3 peripheral blood IL-6 and TNF-α concentration were greater than group D2 reduction(P<0.05). Conclusions LPS can promote isolated human peripheral blood inflammatory cytokine IL-6 and TNF-α concentration increasing. Sufentanil inhibited LPS-induced, IL-6 and TNF-α concentration increase in a dose-dependent manner from the peripheral blood. Sufentanil had no effect on IL-6 and TNF-α concentration the peripheral blood drawn away from people. Key words: Sufentanil; Lipopolysaccharide; Peripheral blood; Interleukin-6; Tumor necrosis factor-α