1.Protective effect of N-acetylcysteine on mice with acute lung injury in-duced by H9N2 swine influenza virus
Ruihua ZHANG ; Cunlian WANG ; Tong XU ; Dong WEI ; Mingju XU ; Baojian LIU ; Guohua WANG ; Shufei TIAN
Chinese Journal of Pathophysiology 2014;33(4):698-705
AIM:To investigate the effects of N-acetylcysteine (NAC) on acute lung injury induced by H9N2 swine influenza virus ( SIV) in mice.METHODS: BALB/c mice were used to establish the animal model of acute lung injury by nasal inoculation of H9N2 SIV.The mice were divided into control group (without SIV infection), H9N2 SIV group (inoculation of H9N2 SIV) and NAC group (inoculation of H9N2 SIV plus pretreatment with NAC).The pulmonary edema was evaluated by determining the lung wet weight /dry weight ( W/D) ratio.The pathological changes of the lung tis-sues were observed .The concontrations of TNF-α, IL-1βand IL-6 in bronchoalveolar lavage fluid ( BALF) were meas-ured.The virus titer, T-SOD activity, MPO activity and MDA content in the homogenate of the lung tissues were detected . RESULTS:Treatment with NAC decreased the morality of infected mice , and significantly prolonged the survival time of infected mice .The pathological changes of the lung tissues , the lung W/D ratio and the lung index were relieved when SIV infected the mice treated with NAC .Treatment with NAC significantly decreased the infiltration of inflammatory cells inclu-ding 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 NAC also significantly increased the T-SOD activity.CONCLUSION: The protective effect of NAC on the acute lung injury mouse model is related to suppression of the oxidative stress and inflamma -tory responses .
2.Kaempferol attenuates acute lung injury in mice induced by swine-origin influenza A H9 N2 virus via down-regulation of NF-κB signaling pathway
Yan LI ; Chunfu WANG ; Ruihua ZHANG ; Cunlian WANG ; Tong XU ; Mingju XU ; Baojian LIU ; Guohua WANG ; Shufei TIAN
Chinese Journal of Pathophysiology 2017;33(2):315-321
[ 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.