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Protocatechuic acid attenuates angiotensin II‐induced cardiac fibrosis in cardiac fibroblasts through inhibiting the NOX4/ROS/p38 signaling pathway
Author(s) -
Song Hui,
Ren Jie
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6435
Subject(s) - nox4 , angiotensin ii , ctgf , cardiac fibrosis , nicotinamide adenine dinucleotide phosphate , myofibroblast , fibrosis , nadph oxidase , reactive oxygen species , myocardial fibrosis , chemistry , microbiology and biotechnology , biology , endocrinology , medicine , growth factor , biochemistry , oxidase test , enzyme , receptor
Cardiac fibrosis plays a crucial role in the pathogenesis of myocardial infarction (MI). It has been found that differentiation of cardiac fibroblasts (CFs) into myofibroblasts is a major event in the process of cardiac fibrosis. In the present study, we aimed to investigate the effects of protocatechuic acid (PCA), a cardiac protective agent, on the CFs differentiation in vitro. The results showed that PCA exhibited inhibitory effects on the cell proliferation and migration in angiotensin II (Ang II)‐induced CFs. PCA treatment suppressed the Ang II‐induced expression of α‐smooth muscle actin (α‐SMA), which is a hallmark of myofibroblasts. In addition, the production of extracellular matrix (ECM) proteins, including type I collagen (Col I) and connective tissue growth factor (CTGF), were significantly decreased in the PCA‐treated CFs. The Ang II‐induced increased levels of matrix metalloproteinase (MMP)‐2, and MMP‐9 were reduced by PCA. Furthermore, PCA resulted in decrease in reactive oxygen species (ROS) generation, as well as the expressions of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme 4 (NOX4) and p‐p38 in Ang II‐induced CFs. These findings showed that PCA treatment prevented the Ang II‐induced cardiac fibrosis by inhibiting the NOX4/ROS/p38 signaling pathway in vitro, suggesting that PCA might be a therapeutic agent for MI.