It inhibits CFs proliferation via the reduction of oxidative stress in vitro (Wang T. et al., 2015), the mechanism where underlying anti-oxidative stress depends on the inhibition of NOX2 and NOX4 in cardiac hypertrophy, thus decreasing the phosphorylation of JNK and TGF-β1 expression and alleviating cardiac fibrosis (Nakayama et al., 2015). Here, TGFB1 is linked to cardiac hypertrophy.