核因子-κB与腹部开放伤合并海水浸泡大鼠全身炎症反应综合征的关系

目的探讨腹部开放伤合并海水浸泡大鼠全身炎症反应综合征（SIRS）发生时核因子-κB（NF-κB）的活性与SIRS的关系。方法采用腹部开放伤合并海水浸泡大鼠致伤模型并诱发SIRS。酶联免疫吸附（ELISA）法检测血肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）水平，免疫组化技术检测NF—κB在外周血淋巴细胞（PBL）和小肠组织中的活性。结果腹部开放伤后海水浸泡1小时，大鼠出现SIRS；血TNF—α、IL-6水平升高；免疫组化显示大鼠PBL和小肠组织中NF-κB表达的阳性率显著升高，与对照组比较有统计学意义（P〈0．05或P〈0．01）。结论腹部开放伤合并海水浸泡可致大鼠SIRS，NF-κB和细胞因子参与了SIRS的发生、发展。NF-κB的激活介导了TNF—α、IL-6等细胞因子的释放，在SIRS中可能处于中心环节。

Relationship of nuclear factor kappa B and systemic inflammatory response syndrome (SIRS) caused by open abdominal injury and seawater immersion in rats

Objective To explore the relationship of NF-κB＇ s activity and systemic inflammatory response syndrome （SIRS） induced by open abdominal injury and seawater immersion in rats. Methods Rat models with open abdominal injury and seawater immersion were established and SIRS was induced. The levels of TNF-α and IL-6 were examined by enzyme-linked immunosorbent assay （ ELISA ）. NF-κB activity in PBL and intestinal tissues were examined by immunohistochemical staining. Results SIRS was observed after 1 hour of seawater immersion of rats with abdominal injuries; the levels of TNF-α and IL-6 increased;the positive rate of NF-κB＇ s expression in PBL and intestinal tissue increased significantly, which had statistical significance compared with the control groups （ P 〈 0.05 or P 〈 0.01 ）. Conclusion Open abdominal injury and seawater immersion can cause SIRS in rats. NF-κB,TNF-α and IL-6 involve in the occurrence and development of SIRS. The activation of NF-κB mediates the release of TNF-α and IL-6 and might play a central role in SIRS.