AB23A Reduces TGF-beta 1-Induced Human Cardiac Fibroblasts (HCF) Proliferation and Collagen Secretion via MER/ ERK1/2/CREB Pathway

摘要

Background and Objectives: Myocardial fibrosis is associated with many forms of heart diseases which is characterized by the accumulation of activated cardiac fibroblasts (CFBs) and excess deposition of extracellular matrix (ECM). Natural compounds such as Alisol B 23-acetate has been proved to maintain the activation of ERK1/2, but whether it can affect cardiac fibroblasts by MER/ERK1/2/CREB signaling pathway is still unknown. Methods: The cell was identified with alpha-SMA protein level detected by immunofluorescence staining method. The cell proliferation was examined by CCK8 assay. Col I and Col III protein levels were examined by western blot and sirius red staining to detect the ECM level. Furthermore, p-MERK, MERK, P-ERK, ERK and CREB were examined by western blot to verify whether Alisol could activate the MERK/ERK1/2/CREB pathway in myocardial fibrosis. Results: CCK8 assay result indicated that Alisol reduced the cell viability of CFBs induced by TGF-beta 1. In addition, Alisol significantly decreased the ECM deposition of CFBs. Furthermore, Alisol could activate MERK/ERK1/2/CREB signaling pathway. Conclusion : These results verified that Alisol inhibited myocardial fibrosis via MERK/ERK1/2/CREB pathway.