Effect of isoliensinine on cardiac fibrosis induced by pressure overload and its mechanism

AimTo investigate the effect of isoliensinine (IL)on myocardial fibrosis induced by pressure overload in mice and to reveal its underlying mechanism.MethodsA pressure-overload myocardial fibrosis model was established in mice by using transverse aortic constriction(TAC), and the mice were divided into four groups: sham operation + vehicle control group(Sham+Vehicle), surgery + vehicle control group(TAC+Vehicle), sham operation + isoliensinine group (Sham+IL), and surgery + isoliensinine group (TAC+IL). WGA staining, Masson staining, Tunel apoptosis detection, immunofluorescence and Western blot were used to detect the degree of myocardial fibrosis, collagen deposition and expression of key proteins in the pathway.ResultsIL intervention could inhibit TAC-induced cardiomyocyte hypertrophy, reduce cardiomyocyte apoptosis, improve myocardial fibrosis, and inhibit collagen Ⅲ deposition. Western blot results showed that IL significantly down-regulated the expression of collagen Ⅰ, collagen Ⅲ, p-Smad2/3, and β -catenin proteins.ConclusionsIL inhibits the activity of TGF-β/Smad and Wnt/β-catenin pathways, reduces abnormal collagen deposition, and improves myocardial remodeling caused by pressure overload, providing a theoretical basis for targeted treatment of pathological myocardial fibrosis.