NDLI: Genistein Alleviates Radiation-Induced Pneumonitis by Depressing Ape1/Ref-1 Expression to Down-regulate Inflammatory Cytokines

Content Provider	Springer Nature Link
Author	Liu, Guo Dong Xia, Lei Zhu, Jian Wu Ou, Shan Li, Meng Xia He, Yong Luo, Wei Li, Juan Zhou, Qian Yang, Xue Qin Shan, Jin Lu Wang, Ge Wang, Dong Yang, Zhen Zhou
Copyright Year	2014
Abstract	The aim of the study was to investigate the role of genistein in alleviating radiation-induced pneumonitis (RIP) through down-regulating levels of the inflammatory cytokines by inhibiting the expression of apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ape1/Ref-1). Fifty female C57BL/6J mice (8 weeks old) were randomly divided into a control group, a pure irradiation (IR) group and a genistein + IR group. At the four time points after IR, hematoxylin, and Masson’s trichrome stainings were used to examine the pathological changes and collagen fiber deposition. Flow cytometry was used to detect reactive oxygen system (ROS) changes, EMSA was used to estimate the nuclear factor kappa B (NF-κB) transcriptional activities and an ELISA assay was used to measure the levels of TGF-β1, IL-1β, TNF-α, and IL-6 in the serum and bronchoalveolar lavage fluid (BALF) 2 weeks after IR. The pathological detection results showed acute inflammatory/fibrinoid exudation of the thoracic tissue after IR, which was significantly alleviated with genistein. The IR-induced an APE1 protein expression increase and NF-κB was effectively suppressed by genistein (P < 0.05). The induction of the inflammatory cytokines TGF-β1, IL-1β, TNF-α, and IL-6 by IR were in turn inhibited in the serum and BALF of the genistein-pretreated mice (P < 0.05). In addition, the ROS production was significantly boosted in the A549 cells after IR, which could be down-regulated by the pretreatment of genistein. The results demonstrate that genistein alleviates RIP by attenuating the inflammatory response in the initiation of RIP. A possible target of genistein is the Ape1/ref-1, which regulates key inflammatory cytokines by activating the NF-κB.
Starting Page	725
Ending Page	733
Page Count	9
File Format	PDF
ISSN	10859195
Journal	Cell Biochemistry and Biophysics
Volume Number	69
Issue Number	3
e-ISSN	15590283
Language	English
Publisher	Springer US
Publisher Date	2014-03-23
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Genistein Radiation-induced thoracic injury Reactive oxygen species AP endonuclease/redox factor-1 NF-κB Cytokines Biochemistry Pharmacology/Toxicology Biotechnology Cell Biology Biophysics and Biological Physics
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Biophysics

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