Beraprost sodium attenuates the development of myocardial fibrosis after myocardial infarction by regulating GSK-3β expression in rats.

ABSTRACT:

Objective

The aim of this study was to elucidate the mechanism of beraprost sodium (BPS) in the intervention of myocardial fibrosis after myocardial infarction (MI) through glycogen synthase kinase-3β (GSK-3β) and to provide new ideas for intervention in myocardial fibrosis.

Materials and methods

MI model rats given BPS and cardiac fibroblasts (CFs) treated with BPS and TGF-β. HE staining and Masson staining were used to detect the pathological changes of myocardial tissue. Fibrotic markers were detected by immunohistochemical staining. The expressions of GSK-3β, cAMP response element binding protein (CREB), and p-CREB were analyzed by qPCR and western blot analysis. EDU staining was used to detect the proliferation of CFs. The promoter activity of GSK-3β was detected by luc

SUBMITTER: Li XX 

PROVIDER: S-EPMC10633815 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature