Abstract
To investigate the effect of inhibitor κBα (IκBα) on severe pneumonia and explain the mechanisms of nuclear factor κB (NF-κB), the activation of NF-κB was induced in Sprague-Dawley (SD) rats infected with Klebsiella pneumoniae (K. pneumoniae). The rats were then treated with differing concentrations of IκBα protein. A histological analysis was performed to compare the lung structure prior to and following treatment, and an immunohistochemistry assay was used to detect NF-κB activity. In addition, the expression of certain inflammatory factors was detected using a protein chip assay. The severe pneumonia rat model was successfully produced and in model rats, NF-κB was activated by K. pneumoniae. Following treatment with IκBα, the activity of NF-κB was inhibited and pneumonia symptoms in model rats were alleviated. Furthermore, the expression of a number of inflammatory factors including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), interferon γ (IFN-γ) and monocyte chemoattractant protein-1 (MCP-1) were also inhibited. The current study demonstrates that NF-κB inhibition with IκBα protein therapy prevents the development of pneumonia in a K. pneumoniae rat model. The therapeutic effect is indicated by the responses of proinflammatory factors, including TNF-α, IL-6, IFN-γ and MCP-1.