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Regulation of Eclipta prostrata L. components on cigarette smoking‐induced autophagy of bronchial epithelial cells via keap1‐Nrf2 pathway
Author(s) -
Ding Shumin,
Hou Xuefeng,
Wang Fujing,
Wang Gang,
Tan Xiaobin,
Liu Ying,
Zhou Yuanli,
Qiu Huihui,
Sun E.,
Jiang Nan,
Li Zihao,
Song Jie,
Feng Liang,
Jia Xiaobin
Publication year - 2018
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22567
Subject(s) - autophagy , transfection , keap1 , microbiology and biotechnology , cytoplasm , downregulation and upregulation , chemistry , atg5 , oxidative stress , biology , apoptosis , biochemistry , gene , transcription factor
Cigarette smoking extract (CSE)‐induced autophagic injury has been regarded as an important contributor to the pathogenesis of lung cancer. We previously found that Eclipta prostrata L. component (CCE) reduced CSE‐induced bronchial epithelial cells damage. However, the mechanism remains unknown. Human normal bronchial epithelial cells (NHBE) were exposed to CSE to establish stress model. Nrf2‐siRNA and Keap1‐siRNA transfection were performed. mRFP‐GFP‐LC3 dual fluorescence and transmission electron microscopy were used to observe the autophagic characteristics. CCE prevented CSE‐induced Nrf2 transfer into cytoplasm and up‐regulated Keap1 level of NHBE cells. Furthermore, CCE significantly increased p‐p16, p‐p21 and p‐p53 phosphorylation levels in Nrf2‐siRNA‐ or Keap1‐siRNA‐transfected cells. As demonstrated by transmission electron microscopy and mRFP‐GFP‐LC3 dual fluorescence assays, CCE mitigated autophagic injury, and also down‐regulated autophagy‐related Beclin‐1, LC3II/LC3I ratio, Atg5 and ATF4 levels. Our findings showed the attenuation of CCE on CSE‐induced NHBE cells injury was associated with Nrf‐2‐mediated oxidative signaling pathway.