Role of nuclear transcription factor-kappaB in endotoxin-induced shock in rats

J Huazhong Univ Sci Technolog Med Sci. 2005;25(2):174-7. doi: 10.1007/BF02873569.

Abstract

To investigate the role of NF-kappaB in endotoxic shock in rats, the model of endotoxin-shock rats was induced by intravenous infusion of lipopolysaccharide (LPS). 1 h, 2 h, 4 h and 6 h after LPS injection, the activation of NF-kappaB in blood mononuclear cells and the content of TNF-alpha and IL-6 in plasma was detected by enzyme-linked immunoadsordent assay (ELISA). The level of mean arterial pressure (MAP) and the histopathological changes of lung and liver were also observed. The activation of NF-kappaB in mononuclear cells increased 1 h after LPS injection and reached its peak 2 h after the injection, and its level was higher than that of normal group. The level of TNF-alpha was increased 1 h after the infusion and peaked 2 h after the injection, and its level was higher than that of normal group after LPS infusion. The content of IL-6 increased gradually with time, the IL-6 level was higher than that of normal group after LPS injection. MAP was decreased gradually with time and its level was lower than that of normal group after LPS injection. Pathological examination showed that endotoxic shock could cause pulmonary alveolar hemorrhage, edema and infiltration of inflammatory cell in lung tissue and congestion, edema, capillary dilation and inflammatory cell infiltration in liver tissue. It is concluded that NF-kappaB can up-regulate the expression of TNF-alpha and IL-6 in plasma and play an important role in endotoxin-induced shock in rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Interleukin-6 / blood*
  • Lipopolysaccharides
  • Male
  • NF-kappa B / metabolism*
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Shock, Septic / chemically induced
  • Shock, Septic / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha