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
): 1398-1402
PMID28413484
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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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