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目的研究干预泛素-蛋白酶体途径对烫伤脓毒症大鼠肺脏核因子-(?)B(NF-(?)B)活化、肿瘤坏死因子-α的产生以及髓过氧化物酶(MPO)活性的影响。方法采用30%TBSAⅢ度烫伤加内毒素攻击大鼠为模型模拟临床烫伤脓毒症,72只Wistar大鼠随机分为正常对照组、烫伤脓毒症组、烫伤脓毒症+蛋白酶体抑制剂N-Acetyl-leucinyl-leucinyl-norleucinal(ALLN)组、烫伤脓毒症+NF-(?)B抑制剂吡咯烷二硫基甲酸酯(Pyrrolidine Dithiocarbamate．PDTC)组,采用凝胶电泳迁移率改变分析法(EMSA)分析肺脏NF-(?)B活性,采用酶联免疫吸附试验检测肺脏TNF-α的变化,采用分光光度法检测肺组织髓过氧化物酶(MPO)的活性。结果肺组织NF-(?)B活性于伤后1h明显增强达到高峰(P＜0．01),伤后2h仍保持较高的活化水平,之后呈逐渐下降趋势。PDTC可明显降低其在伤后1h和2h的活性(P＜0．01),而ALLN可明显降低其在伤后1h的活性(P＜0．01)。PDTC两种抑制剂均可明显降低伤后2h肺组织TNF-α产生,明显降低伤后2h和6h肺组织MPO的活力(P＜0．01)。结论蛋白酶体抑制剂可降低烫伤脓毒症大鼠肺组织NF-(?)B的活性。降低肺组织的炎症反应。
Objective To investigate the effects of intervention of ubiquitin - proteasome pathway on activation of NF - κB, production of tumor necrosis factor - α (TNF - α) and myeloperoxidase (MPO) in the lungs of scalded septic rats. Effect of activity. Methods 30% TBSA Ⅲ degree scald plus endotoxin challenge rats were used to model clinical scalded sepsis. 72 Wistar rats were randomly divided into normal control group, scalded sepsis group, scalded sepsis + proteasome inhibitor N The rats were randomly divided into 4 groups: control group, Acetyl-leucinyl-leucinyl-norleucinal (ALLN) group, scald sepsis + NF - B inhibitor Pyrrolidine Dithiocarbamate.PDTC group. The activity of NF -? B in lung tissue was analyzed by EMSA. The level of TNF - α in lung was detected by enzyme linked immunosorbent assay (ELISA). The activity of myeloperoxidase (MPO) in lung tissue was detected by spectrophotometry. Results The activity of NF -? B in lung tissue increased significantly (P <0.01) 1 h after injury and remained high at 2 h after injury, and then gradually decreased. PDTC significantly decreased its activity at 1 h and 2 h after injury (P <0.01), while ALLN significantly reduced its activity 1 h after injury (P <0.01). PDTC both could significantly reduce the production of TNF-α in lung tissue 2h after injury, and significantly reduce the activity of MPO in lung tissue 2h and 6h after injury (P <0.01). Conclusion Proteasome inhibitors can reduce the activity of NF -? B in the lungs of scalded sepsis rats. Reduce the inflammation of the lung tissue.