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Chinese Journal of Pathophysiology ; (12): 315-321, 2017.
Article in Chinese | WPRIM | ID: wpr-506341

ABSTRACT

[ ABSTRACT] AIM:To investigate whether kaempferol protects against acute lung injury induced by swine -origin influenza A H9N2 virus via down-regulation of NF-κB signaling pathway .METHODS:BALB/c mice were used to estab-lish the animal model of acute lung injury by nasal inoculation of swine-origin influenza A H9N2 virus.After the interven-tion with kaempferol , the pulmonary edema was evaluated by determining the lung wet weight /dry weight ( W/D) ratio, the pathological changes of the lung tissues were observed , the concentrations of TNF-α, IL-1βand IL-6 in the bronchoalveolar lavage fluid (BALF) were measured, and superoxide dismutase (SOD) activity, myeloperoxidase (MPO) activity and MDA content in the homogenate of the lung tissues were detected .NF-κB P65 levels were determined by Western blot , and the NF-κB P65 and NF-κB P50 nuclear translocation in the nuclear extracts from mouse lung tissue homogenate was detec-ted by ELISA .RESULTS:Treatment with kaempferol decreased the morality of infected mice , and significantly prolonged the survival time of the infected mice .Kaempferol also relieved the pathological changes of the lung tissues , the lung W/D ratio and the lung index in swine-origin influenza A H9N2 virus-infected mice.Treatment with kaempferol significantly de-creased the infiltration of inflammatory cells including macrophages , lymphocytes and neutrophils in the BALF .The levels of TNF-α, IL-6, IL-1βand MDA and the activity of MPO were also decreased .Treatment with kaempferol also significantly increased the SOD activity .NF-κB P65 levels were decreased , and the NF-κB P65 and NF-κB P50 nuclear translocation in the nuclear extracts from the mouse lung tissue homogenate were also decreased by treatment with kaempferol .CONCLU-SION:The protective effect of kaempferol on the mice with acute lung injury induced by swine -origin influenza A H9N2 vi-rus is related to suppression of the oxidative stress and inflammatory responses by down-regulation of NF-κB signaling path-way.

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