In this study, the inhibitory effect of BEL on myocardial fibrosis has been confirmed for the first time, and the relevant molecular mechanism has been clarified, which may be related to the inhibition of the proliferation and phenotypic transformation of CFs by regulating TGF-β1/Smads and p38 signaling and preventing NR4A1 cytoplasmic localization. The gene discussed is NR4A1; the disease is Myocardial fibrosis.