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10.3892/etm.2017.4130

http://scihub22266oqcxt.onion/10.3892/etm.2017.4130
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C5377337!5377337!28413484
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suck abstract from ncbi


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pmid28413484      Exp+Ther+Med 2017 ; 13 (4): 1398-402
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  • Inhibitor ?B? protein therapy alleviates severe pneumonia through inhibition of nuclear factor ?B #MMPMID28413484
  • Xu H; Mei B; Wang M; Xu S
  • Exp Ther Med 2017[Apr]; 13 (4): 1398-402 PMID28413484show ga
  • To investigate the effect of inhibitor ?B? (I?B?) on severe pneumonia and explain the mechanisms of nuclear factor ?B (NF-?B), the activation of NF-?B was induced in Sprague-Dawley (SD) rats infected with Klebsiella pneumoniae (K. pneumoniae). The rats were then treated with differing concentrations of I?B? 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-?B 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-?B was activated by K. pneumoniae. Following treatment with I?B?, the activity of NF-?B was inhibited and pneumonia symptoms in model rats were alleviated. Furthermore, the expression of a number of inflammatory factors including tumor necrosis factor ? (TNF-?), interleukin 6 (IL-6), interferon ? (IFN-?) and monocyte chemoattractant protein-1 (MCP-1) were also inhibited. The current study demonstrates that NF-?B inhibition with I?B? 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-?, IL-6, IFN-? and MCP-1.
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