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.

Objective To evaluate the effect of oxycodone on microglial activation in brain tissues of rats. Methods Primarily cultured microglial cells of Sprague?Dawley rats were seeded in 24?well plates (1 ml∕well)at a density of 1×105cells∕ml and divided into 5 groups(n=40 each)using a random num?ber table: control group(group C), lipopolysaccharide(LPS)group(group L)and low, medium and high concentrations of oxycodone groups(O25, O50, O100groups). The cells were cultured in serum?free medium for 24 h in group C. LPS was added at the final concentration of 1 μg∕ml in L, O25, O50and O100 groups, and in addition oxycodone was added at the final concentration of 25, 50 and 100 ng∕ml at 24 h of incubation with LPS in O25, O50and O100groups, respectively. Cells were collected at 1 h of incubation or culture for determination of the expression of tumor necrosis factor?α(TNF?α), interleukin?1β(IL?1β), IL?10 and transforming growth factor?1β(TGF?1β)mRNA(by real?time polymerase chain reaction)and expression of TGF?1β and phosphorylated Smad2(p?Smad2)(using Western blot). The concentrations of TNF?α, IL?1β and IL?10 in the supernatant were detected by enzyme?linked immunosorbent assay. Results Compared with group C, the expression of TGF?β1, IL?1β and TNF?α mRNA, TGF?β1 and p?Smad2 was significantly up?regulated, and the concentrations of IL?1β, IL?10 and TNF?α in the supernatant were increased in group L(P<0.01). Compared with group L, the expression of TGF?β1, IL?1β and TNF?α mRNA, TGF?β1 and p?Smad2 was significantly down?regulated in O50and O100groups, the expression of IL?10 mRNA was significantly up?regulated, and the concentrations of IL?1β and TNF?α in the supernatant were decreased in group O100(P<0.05), and no significant change was found in the parameters mentioned above in group O25(P>0.05). Conclusion Oxycodone can inhibit microglial activation in brain tissues of rats.

Objective To evaluate the effect of dexmedimidine on intestinal injury in rats with endotoxemia.Methods Twenty-four healthy adult male Sprague-Dawley rats,aged 2-3 months,weighing 200-250 g,were divided into 4 groups (n =6 each) using a random number table method:control group (group C),endotoxemia group (group E),dexmedimidine group (group D) and dexmedimidine plus α7 subunit-containing nicotinic acetylcholine receptor antagonist group (D +α-BGT group).The endotoxemia model was established by injecting lipopolysaccharide (LPS) 10 mg/kg via the femoral vein.Dexmedetomidine 40 μg/kg was injected and 15 min later LPS was intravenously injected in group D.Dexmedetomidine 40 μg/kg was intraperitoneally injected after intraperitoneal injection of α-bungarotoxin 1 μg/kg,and 15 min later LPS was intravenously injected in group D+o-BGT.Blood samples were collected from the abdominal aorta at 6 h after LPS injection for determination of the plasma interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) concentrations (by enzyme-linked immunosorbent assay).Rats were sacrificed after blood sampling,and intestinal tissues were obtained for examination of the pathological changes and for determination of the myeloperoxidase (MPO) activity (by chemical colorimetry) and expression of NF-κB p65 in nucleoprotein (by Western blot).Results Compared with group C,the plasma IL-6 and TNF-o concentrations and MPO activity in intestinal tissues were significantly increased,and the expression of NF-κB p65 in nucleoprotein was up-regulated in the other 3 groups (P＜0.05).Compared with group E,the plasma IL-6 and TNF-α concentrations and MPO activity in intestinal tissues were significantly decreased,the expression of NF-κB p65 in nucleoprotein was down-regulated (p＜0.05),and the pathological changes of intestinal tissues were significantly attenuated in group D.Compared with group D,the plasma IL-6 and TNF-α concentrations and MPO activity in intestinal tissues were significantly increased,the expression of NF-κB p65 in nucleoprotein was up-regulated (P＜0.05),and the pathological changes of intestinal tissues were accentuated in group D+α-BGT.Conclusion Dexmedetomidine can reduce the intestinal injury in rats with endotoxemia,and the mechanism may be related to activating cholinergic anti-inflammatory pathway and further inhibiting inflammatory responses.