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Biomed Pharmacother. 2017 May;89:660-672. doi: 10.1016/j.biopha.2017.02.081. Epub 2017 Mar 3.

Kaempferol ameliorates H9N2 swine influenza virus-induced acute lung injury by inactivation of TLR4/MyD88-mediated NF-κB and MAPK signaling pathways.

Author information

1
Key Laboratory of Preventive Veterinary Medicine, Department of Veterinary Medicine, Animal Science College, HeBei North University, Zhangjiakou 075131, China.
2
College of Animal Science and Veterinary Medicine, Tianjin Agricultural University, Tianjin 300384, China.
3
Army Artillery Training Base, Xuanhua 075100, China.
4
The Eighth Hospital of Shijiazhuang, Shijiazhuang 050000, China.
5
Key Laboratory of Preventive Veterinary Medicine, Department of Veterinary Medicine, Animal Science College, HeBei North University, Zhangjiakou 075131, China. Electronic address: xutong1969@sohu.com.
6
Huang Yang Cheng Central School, ChaYouZhongQi, Wulanchabu City, Inner Mongolia 013550, China.
7
Qianjin Farm of Jiansanjiang Administration of Heilongjiang Province, Heilongjiang 156331, PR China.

Abstract

Kaempferol, a very common type of dietary flavonoids, has been found to exert antioxidative and anti-inflammatory properties. The purpose of our investigation was designed to reveal the effect of kaempferol on H9N2 influenza virus-induced inflammation in vivo and in vitro. In vivo, BALB/C mice were infected intranasally with H9N2 influenza virus with or without kaempferol treatment to induce acute lung injury (ALI) model. In vitro, MH-S cells were infected with H9N2 influenza virus with or without kaempferol treatment. In vivo, kaempferol treatment attenuated pulmonary edema, the W/D mass ratio, pulmonary capillary permeability, myeloperoxidase (MPO) activity, and the numbers of inflammatory cells. Kaempferol reduced ROS and Malondialdehyde (MDA) production, and increased the superoxide dismutase (SOD) activity. Kaempferol also reduced overproduction of TNF-α, IL-1β and IL-6. In addition, kaempferol decreased the H9N2 viral titre. In vitro, ROS, MDA, TNF-α, IL-1β and IL-6 was also reduced by kaempferol. Moreover, our data showed that kaempferol significantly inhibited the upregulation of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), phosphorylation level of IκBα and nuclear factor-κB (NF-κB) p65, NF-κB p65 DNA binding activity, and phosphorylation level of MAPKs, both in vivo and in vitro. These results suggest that kaempferol exhibits a protective effect on H9N2 virus-induced inflammation via suppression of TLR4/MyD88-mediated NF-κB and MAPKs pathways, and kaempferol may be considered as an effective drug for the potential treatment of influenza virus-induced ALI.

KEYWORDS:

Acute lung injury; Kaempferol; MAPKs; Nuclear factor-kappaB; Toll-like receptor 4

PMID:
28262619
DOI:
10.1016/j.biopha.2017.02.081
[Indexed for MEDLINE]

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