基础医学与临床 ›› 2010, Vol. 30 ›› Issue (11): 1202-1205.

• 研究论文 • 上一篇    下一篇

急性胰腺炎患者高迁移率族蛋白B1表达增强

卢干珍 吴传新 刘杞 龚建平 孙航   

  1. 重庆医科大学病毒性肝炎研究所 重庆医科大学附属第二医院肝胆外科
  • 收稿日期:2010-05-11 修回日期:2010-07-14 出版日期:2010-11-05 发布日期:2010-11-05

Increased expression of high-mobility group box chromosomal protein 1 in patients with acute pancreatitis

Gan-zhen LU, Chuan-xin WU, Qi LIU, Jian-ping GONG, Hang SUN   

  1. Chongqing Medical University the Second Affiliated Hospital
  • Received:2010-05-11 Revised:2010-07-14 Online:2010-11-05 Published:2010-11-05

摘要: 目的 探讨高迁移率族蛋白B1(HMGB1)在急性胰腺炎(AP)中的表达及其临床意义。方法 选择轻症急性胰腺炎(MAP)20例,重症急性胰腺炎无器官功能障碍(SAP-1)10例,伴器官功能障碍(SAP-2)10例,健康志愿者20例,用RT-PCR检测血液中HMGB1 mRNA水平、用ELISA检测血清中HMGB1、TNF-α和IL-6的浓度,分析血清HMGB1水平与急性胰腺炎病情严重程度的关系。结果 MAP组、SAP-1组、SAP-2组血清中HMGB1的浓度分别为3.5 ± 0.8、5.7 ± 1.6 和8.3 ± 1.7 ng/mL,明显高于对照组的1.6 ± 0.4 ng/mL; HMGB1 mRNA的表达分别为0.56±0.11,0.71±0.07和0.89±0.09,明显高于对照组的0.25±0.04。HMGB1的表达均随病情加重而增加。结论 HMGB1在重症急性胰腺炎的病理过程中起十分重要的作用,并且可能是其发生器官功能障碍的一种关键性的细胞因子。

Abstract: Objective To investigate the expression of high-mobility group box chromosomal protein 1(HMGB1) in patients with acute pancreatitis (AP) and its clinical value. Methods We measured blood HMGB1 mRNA levels by RT-PCR and serum HMGB1,TNF-α and IL-6 concentrations by an enzyme-linked immunosorbent assay in 20 patients with mild AP (MAP), 10 patients of severe acute pancreatitis without organ dysfunction (SAP-1), 10 patients of SAP with organ dysfunction (SAP-2). Furthermore, relationship between their serum HMGB1 levels and severity of AP was analyzed. Results The mean value of serum HMGB1 concentrations in patients with MAP, SAP-1 and SAP-2 were 3.5 ± 0.8 , 5.7 ± 1.6 and 8.3 ± 1.7 ng/mL respectively and were significantly higher than that in healthy subjects 1.6 ± 0.4 ng/mL. Blood HMGB1 mRNA levels in patients with MAP, SAP-1 and SAP-2 were 0.56±0.11,0.71±0.07,0.89±0.09 respectively and were significantly higher than that in healthy subjects 0.25±0.04. Serum HMGB1 levels and HMGB1 mRNA were significantly increased in patients with AP and were correlated with disease severity. Conclusion These results suggest that HMGB1 may act as a key mediator for inflammation and organ failure in AP.