Effects of postconditioning with propofol on lipopolysaccharide-induced inflammatory responses of microglial cells in rat brain tissues

Objective To evaluate the effects of postconditioning with propofol on lipopolysaccharide (LPS)-induced inflammatory responses of microglial cells in rat brain tissues.Methods The primary cultured microglial cells in brain tissues of Sprague-Dawley rats were seeded in 24 multi-well plates at a density of 1 × 105 cells/ml,and the microglial cells of 100 wells were randomly divided into 5 groups (n =20 each) using a random number table:control group (group C),LPS group (group L),and propofol 25,50 and 100 μmol/L groups (P25,P50,P100 groups).The cells were cultured routinely in group C.LPS 1 μg/ml was added and the cells were incubated for 24 h in group L.In P25,P20,and P100 groups,when the cells were incubated for 24 h with LPS 1 μg/ml,propofol with the final concentrations of 25,50 and 100 μmol/L was added,respectively.The cells were collected at 1 h of incubation with propofol for determination of the expression of inducible nitric oxide synthase (iNOS) mRNA,cyclooxygenase-2 (COX-2) mRNA,tumor necrosis factor-α (TNF-α) mRNA and interleukin-1β (IL-1β) mRNA (by RT-PCR).The supematant was separated for determination of the concentrations of nitric oxide (NO) (by Griess method) and pmstaglandin E2 (PGE2),TNF-α and IL-1β (by ELISA).Results Compared with group C,the expression of iNOS mRNA,COX-2 mRNA,TNF-α mRNA and IL-1β mRNA was significantly up-regulated and the concentrations of NO,PGE2,TNF-α and IL-1β in the supematant were increased in group L (P ＜ 0.01).Compared with group L,the expression of iNOS mRNA,COX-2 mRNA,TNF-α mRNA and IL-1β mRNA was significantly down-regulated and the concentrations of NO,PGE2,TNF-α and IL-1β in the supernatant were decreased in P50 and P100 groups (P ＜ 0.05 or 0.01),while no significant change in the indexes mentioned above was found in P25 group (P ＞ 0.05).Conclusion Postconditioning with propofol 50 and 100 μmol/L can inhibit LPS-induced inflammatory responses of microglial cells in rat brain tissues. Key words: Propofol;  Microglia;  Endotoxemia;  Inflammation