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Piperlongumine inhibits angiotensin II‐induced extracellular matrix expression in cardiac fibroblasts
Author(s) -
Wu Xianchuang,
Liu Yuxin,
An Jihong,
Li Jiahuan,
Lv Weiling,
Geng Shengnan,
Zhang Yongzhou
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27379
Subject(s) - angiotensin ii , extracellular matrix , cardiac fibrosis , reactive oxygen species , myofibroblast , chemistry , microbiology and biotechnology , extracellular , myocardial fibrosis , cell growth , p38 mitogen activated protein kinases , fibrosis , matrix metalloproteinase , signal transduction , phosphorylation , pharmacology , biology , medicine , biochemistry , protein kinase a , receptor
Piperlongumine (PL), a single component isolated from Piper longum , has been reported to possess anti‐inflammatory, antibacterial, antiangiogenic, antioxidant, antitumor, and antidiabetic activities. However, its role in cardiac fibrosis remains to be clarified. Therefore, we determined the effects of PL on cardiac fibroblasts (CFs) proliferation, and extracellular matrix (ECM) production under angiotensin II (Ang II) conditions, and further investigated the underlying molecular mechanism. Our data revealed that PL inhibited the proliferation and migration of CFs induced by Ang II. In addition, PL blocked the transformation of CFs to myofibroblasts induced by Ang II, as well as decreased cellular reactive oxygen species (ROS) production and malondialdehyde level in Ang II‐stimulated CFs. Furthermore, PL significantly suppressed the Ang II‐increased phosphorylation of extracellular regulated protein kinase 1/2 (ERK1/2) in CFs. Taken together, the results of the current study demonstrated that PL inhibits Ang II‐induced cell proliferation, migration, and ECM expression in CFs through the inactivation of the ERR1/2 signaling pathway. These data strongly suggest that PL may be a promising therapeutic candidate for the treatment of cardiac fibrosis.