Effects of paeonol on proliferation and collagen synthesis of rat cardiac fibroblasts induced by aldosterone

Abstract

The aim of this study was to explore the possible molecular mechanisms of paeonol in preventing ventricular remodeling. The cell viability of neonatal rat cardiac fibroblasts was detected by the method of MTT. RT-PCR and Western blot were used to measure the expression of TGF-β1, type I collagen and type III collagen. After treating the cardiac fibroblasts with paeonol, the cell viability decreased (p<0.01), and the expression of TGF-β1, type I collagen and types III collagen was significantly reduced (p<0.01). Thus, paeonol can inhibit the proliferation of fibroblast cells induced by aldosterone. The molecular mechanism is related to the down-regulation of TGF-β1 and type I and III collagen gene expression.

Q-myocardial Infarction on the Background of Undifferentiated Connective Tissue Dysplasia: Pathogenetic “Paradoxes” and “Crossovers”

“…Because microfilaments are proteinaceous and have an amino acid composition synonymous with collagen and other connective tissue structures, changes in platelet function are expected in patients with UCTD. Decreased platelet levels and changes in their aggregation potential seem to lead to a weakening of arterial thrombogenesis, but deviations in the morphology of such platelets create the preconditions for endothelial microtrauma and ultimately enhance thrombogenesis [11,17,18]. Thus, changes in the cytoskeleton of platelets associated with depolarization of actin and disruption of calcium homeostasis in the cell are accompanied by disruption of their pre-aggregation transformation and serotonin release.…”