RESUMO
OBJECTIVE: Mice injected with Bacillus Calmette-Guérin (BCG) were challenged with lipopolysaccharide (LPS) to induce inflammatory liver injury. This study was performed to explore the protective effects of interleukin (IL)-4 against liver injury induced by BCG and LPS in mice. MATERIALS AND METHODS: Mice injected with BCG (125 mg/kg) were challenged with LPS (10 µg/kg) to induce the model of inflammatory liver injury. Half an hour after injection of LPS, mice were subcutaneously administered rmIL-4 at 5 and 0.5 µg/kg, respectively. Liver injury was evaluated by serum transaminase assay and H & E staining. Liver cytokine concentrations were determined by enzyme-linked immunosorbent assay, and intrahepatic cytokine and iNOS mRNA levels by reverse transcriptase polymerase chain reaction. Intrahepatic apoptosis was evaluated by terminal deoxynucleotidyl transferase mediated nick end labeling. NF-κB p65 and ERK signal pathway was detected by Western-blotting. NF-κB signal pathway was also detected by electrophoretic mobility shift assay. RESULTS: IL-4 reduced the serum ALT, AST and LDH, alleviated the inflammatory cells infiltration, down regulated the expression of TNF-α, IL-1ß, IFN-γ, IL-6 and iNOS mRNA in liver, and alleviated hepatic glutathione depletion (GSH). In addition, IL-4 displayed inhibition of extracellular signal-regulated kinase phosphorylation and NF-κB activation. CONCLUSION: IL-4 may protect mice against BCG/LPS-induced immune liver injury, besides ERK and NF-κB signal pathways were involved in the effects.
Assuntos
Interleucina-4/metabolismo , Lipopolissacarídeos/metabolismo , Mycobacterium bovis/metabolismo , Alanina Transaminase/metabolismo , Animais , Aspartato Aminotransferases/metabolismo , Feminino , Inflamação/tratamento farmacológico , Interferon gama/metabolismo , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , L-Lactato Desidrogenase/metabolismo , Fígado/lesões , Camundongos , Camundongos Endogâmicos BALB C , Óxido Nítrico Sintase Tipo II/metabolismo , RNA Mensageiro/metabolismo , Temperatura , Fator de Necrose Tumoral alfa/metabolismoRESUMO
The self-organization of citrate-capped Au nanoparticles on silicon slide driven by solvent evaporation is carried out under an time-varied magnetic field. The monolayer formation and succedent re-aggregation of Au nanoparticles are observed. The mechanism is proposed based on the interaction between Au colloidal surface and rotating electric field around nanoparticles induced by time-varied magnetic field.