ABSTRACT
Objective To evaluate the role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygen-glucose deprivation(OGD)injury in rat hippocampal slices.Methods Male adult SD rats weighing 80-100 g were anesthetized with ether and decapitated.The hippocampi were removed and sagittally sliced(400μm thick)and placed in artificial cerebrospinal fluid(aCSF)aerated with 95％ O2-5％CO2.Fifty hippoeampal slices were randomly divided into 5 groups(t =10 each):OGD group; 4％ sevoflurane postconditioning group(group Sevo); PD98059(specific inhibitor of ERK)group(group PD); dimethyl sulfoxide (DMSO)group; 4％ sevoflurane postconditioning + PD98059 group(group SPD).OGD was induced by incubating the slices in glucose-free aCSF aerated with 95％ N2-5％ CO2 for 15 min in group OGD.The hippocampal slices were perfused with aCSF saturated with 4％ sevoflurane for 30 min after OGD was induced in group Sevo.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L for 10 min after OGD was induced in group PD.The hippocampal slices were perfused with aCSF containing DMSO 1 mol/L for 10 min after OGD was induced in group DMSO.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L and aerated with 4％ sevoflurane for 30 min after OGD was induced in group SPD.The hippocampal slices were then perfused with plain aCSF for 1 h again in all the groups.The electrophysiological technique was used 1o record the amplitude of orthodromic population spike(OPS)in the stralum pyramidale of the CAI region.TTC staining was used to determine the degree of tissue injury.Results Compared with group OGD,the recovery amplitude and rate of OPS were significantly increased,and the degree of tissue injury was significantly decreased in group Sevo(P ＜0.01),while no significant change was found in each parameter in the other three groups(P ＞ 0.05).Compared with group Sevo,the recovery amplitude and tale of OPS were significandy decreased,and the degree of tissue injury was significantly increased in groups PD,DMSO and SPD(P ＜ 0.01).Conclusion ERK1/2 signal transduction pathway is involved in sevoflurane postcondilioning-induced reduction of OGD injury in tat hippocampal slices.
ABSTRACT
Objective To study the effects of PM2.5 and PM10 of dust storm on the secretion of nitrogen oxide(NO), interleukin-8 (IL-8) and tumor necrosis factor-?(TNF-?)in the alveolar macrophages(AM)of rat in vitro. Methods PM2.5 and PM10 were collected during dust storm period in the urban area of Beijing. The tested cells were primary cultured alveolar macrophages. Cytotoxicity of the particles was measured by MTT assay. The content of NO was determined using Griess reagent. The levels of cytokines IL-8 and TNF-? were determined using radioimmunity assay. Results After treatment for 24 h, PM2.5 and PM10 caused cytotoxicity to AM and the survival rate of the cells was decreased with the increasing exposure dose of the dust to the rats and the survival rate of the cells in the high dosage group was 80% of the control group. At concentrations of 20～150 ?g/ml, PM2.5 and PM10 increased the secretion of NO, TNF-? and IL-8 in AM in a dose-dependent manner. The cytotoxicity of PM2.5 was stronger than that of the PM10 at the same concentration, while the effects on the increasing secretion of NO, IL-8 and TNF-? induced by PM2.5 was smaller than that of the PM10. Conclusion PM2.5 and PM10 of dust storm could induce the secretion of inflammatory factors NO, IL-8 and TNF-? in rat AM.