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目的 研究四氢吡咯二硫代氨基甲酯 (pyrrolidinedithiocarbamate ,PDTC)对抗小鼠全氟异丁烯(perfluoroisobutylene ,PFIB)吸入性急性肺损伤 (acutelunginjury ,ALI)的预防作用机制。方法 采用小鼠动态吸入PFIB周身暴露染毒装置对实验小鼠进行染毒 ,应用电泳泳动分析法 (electrophoreticmobilityshiftassays ,EMSA)检测肺组织核因子 kappaB (nuclearfactor kappaB ,NF κB)的表达情况 ;采用RIA检测血清中IL 1β、IL 8的含量变化。 结果 PFIB吸入染毒后 ,肺组织内NF κB的表达明显高于正常组 ,染毒前 3 0minPDTC ( 12 0mg/kg)预防可以显著抑制NF κB的表达 ;小鼠血清中IL 1β、IL 8的含量在PFIB染毒后显著升高 ,染毒前 3 0minPDTC ( 12 0mg/kg)预防可以显著地抑制这种升高。结论 PDTC对小鼠PFIB吸入性肺损伤具有预防作用可能是基于其对NF κB的抑制 ,进而抑制前炎症细胞因子IL 1β、IL 8等的过度表达 ,从而抑制了过度炎症的进一步发展
Objective To investigate the preventive mechanism of pyrrolidinedithiocarbamate (PDTC) against murine perfluoroisobutylene (PFIB) -induced acute lung injury (ALI). Methods The mice were challenged with PFIB whole body exposed exposure device. The expression of nuclear factor kappaB (NFκB) in lung tissue was detected by electrophoretic mobility shift assay (EMSA) Serum IL 1β, IL 8 levels were measured. Results After PFIB inhalation, the expression of NF-κB in lung tissue was significantly higher than that in normal group. Pretreatment with PDTC at 120 min before exposure could significantly inhibit the expression of NF-κB. The level of IL-1β, IL-8 The content of PFB increased significantly after exposure to PFIB. Prevention of PDTC (120 mg / kg) 30 min before exposure significantly inhibited this increase. Conclusions PDTC can prevent PFIB inhalation lung injury in mice, which may be due to the inhibition of NF κB and the suppression of overexpression of pro-inflammatory cytokines IL 1β and IL 8, thereby inhibiting the further development of excessive inflammation