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IL‐17A‐mediated ERK1/2/p65 signaling pathway is associated with cell apoptosis after non‐alcoholic steatohepatitis
Author(s) -
Pan Yajie,
Ren Xing,
Zhang Yingying,
Lv Jun,
Zeng Qinglei,
Zhang Hongyu,
Yu Zujiang
Publication year - 2019
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1960
Subject(s) - steatohepatitis , apoptosis , signal transduction , pathogenesis , cancer research , microbiology and biotechnology , chemistry , interleukin , fatty liver , cytokine , medicine , biology , immunology , biochemistry , disease
Interleukin (IL)‐17A is pro‐inflammatory cytokine which has been identified as a noninvasive marker of the pathogenesis of non‐alcoholic steatohepatitis (NASH). However, the underlying role of IL‐17A in NASH progression remains unclear. This study was designed to investigate the biological function and molecular mechanism of IL‐17A in the induction of NASH. The results showed that IL‐17A was highly expressed in high‐fat diet (HFD)‐induced NASH mouse model. Intravenous injection of IL‐17A exacerbated steatohepatitis process via promoting hepatocyte apoptosis. Furthermore, IL‐17A‐induced apoptosis was mediated by ERK1/2/p65 signaling pathway. In conclusion, we demonstrated that IL‐17A‐mediated ERK1/2/p65 signaling pathway was a promising target for the treatment of NASH. © 2018 IUBMB Life, 71(3):302–309, 2019