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2. IL‐17A‐mediated ERK1/2/p65 signaling pathway is associated with cell apoptosis after non‐alcoholic steatohepatitis.

Author

Pan, Ya‐jie, Ren, Xing, Zhang, Ying‐ying, Lv, Jun, Zeng, Qing‐lei, Zhang, Hong‐yu, and Yu, Zu‐jiang

Subjects
*FATTY liver, *APOPTOSIS, *INFLAMMATION, *CELL death, *FATTY degeneration
Abstract

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 [ABSTRACT FROM AUTHOR]

Published
2019
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