论文部分内容阅读
目的探讨核因子-κB(NF-κB)在二烯丙基三硫(DATS)抑制脂多糖(LPS)致急性肺损伤(ALI)小鼠IL-1β表达中的作用。方法小鼠随机分为对照组、ALI组、DATS组、DATS预防组和DATS治疗组。RT-PCR检测肺组织中IL-1βmRNA表达。电泳迁移率改变(EMSA)检测肺组织NF-κB活性,Western blot检测肺组织中磷酸化及非磷酸化IκB的表达。结果ALI组小鼠肺组织中IL-1βmRNA表达明显升高(P<0.01),NF-κB活性及磷酸化IκB表达也明显高于对照组(P<0.05)。DATS预防组可显著抑制肺组织中IL-1βmRNA表达(P<0.05)、NF-κB活性及磷酸化IκB表达(P<0.05),但DATS治疗组的抑制效果不明显。结论DATS可通过抑制LPS诱导的IκB磷酸化及随后的NF-κB活化,进而抑制ALI小鼠肺组织IL-1βmRNA表达,这是DATS发挥抗ALI作用的信号传导机制之一。
Objective To investigate the role of nuclear factor-κB (NF-κB) in the inhibition of IL-1β expression by lipopolysaccharide (LPS) -induced acute lung injury (ALI) induced by diallyl trisulfide (DATS). Methods Mice were randomly divided into control group, ALI group, DATS group, DATS prevention group and DATS treatment group. The expression of IL-1βmRNA in lung tissue was detected by RT-PCR. Electrophoretic mobility shift assay (EMSA) was used to detect NF-κB activity in lung tissue. Western blot was used to detect phosphorylated and non-phosphorylated IκB in lung tissue. Results The expression of IL-1βmRNA in lung tissue of ALI group was significantly increased (P <0.01), and the expression of NF-κB and phosphorylated IκB were also significantly higher in ALI group than that in control group (P <0.05). The DATS prevention group could significantly inhibit the expression of IL-1βmRNA (P <0.05), the activity of NF-κB and the phosphorylation of IκB in lung tissue (P <0.05), but the inhibitory effect was not obvious in DATS treatment group. Conclusion DATS can inhibit LPS-induced phosphorylation of IκB and subsequent activation of NF-κB, thereby inhibiting the expression of IL-1βmRNA in the lung tissue of ALI mice. This is one of the signaling pathways by which DATS exerts an anti-ALI effect.