首页> 外文期刊>Inflammation research: Official journal of the European Histamine Research Society >Protective effects of IL-4 on Bacillus Calmette-Guerin and lipopolysaccharide induced immunological liver injury in mice
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Protective effects of IL-4 on Bacillus Calmette-Guerin and lipopolysaccharide induced immunological liver injury in mice

机译:IL-4对卡介苗芽孢杆菌和脂多糖诱导的小鼠免疫性肝损伤的保护作用

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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 enzymelinked 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-1β, 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/LPSinduced immune liver injury, besides ERK and NF-κB signal pathways were involved in the effects.
机译:目的注射卡介苗芽孢杆菌(BCG)的小鼠受到脂多糖(LPS)的刺激,引起炎症性肝损伤。进行这项研究以探讨白介素(IL)-4对BCG和LPS诱导的小鼠肝损伤的保护作用。材料和方法用BPS(10μg/ kg)攻击注射了BCG(125 mg / kg)的小鼠,以诱发炎症性肝损伤模型。注射LPS后半小时,分别以5和0.5μg/ kg皮下注射rmIL-4。通过血清转氨酶测定和H&E染色评估肝损伤。通过酶联免疫吸附测定法测定肝细胞因子浓度,通过逆转录酶聚合酶链反应测定肝内细胞因子和iNOS mRNA水平。通过末端脱氧核苷酸转移酶介导的切口末端标记评估肝内凋亡。 Western blotting检测NF-κBp65和ERK信号通路。电泳迁移率漂移分析也检测到了NF-κB信号通路。结果IL-4降低血清ALT,AST和LDH,减轻炎症细胞浸润,下调肝组织TNF-α,IL-1β,IFN-γ,IL-6和iNOS mRNA的表达,减轻肝谷胱甘肽耗竭(GSH)。此外,IL-4表现出对细胞外信号调节激酶磷酸化和NF-κB活化的抑制作用。结论IL-4可能通过ERK和NF-κB信号通路参与BCG / LPS诱导的免疫性肝损伤。

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