The results suggest that GBE may inhibit experimental myocardial remodeling in rats after acute myocardial infarction by reducing the transcription of TGF-β1, MMP-2 and MMP-9 genes and attenuating extracellular matrix deposition by decreasing the levels of proteins such as type I collagen, MMP-2, and MMP-9 [156]. Here, MMP2 is linked to acute myocardial infarction.