punicalagin and Fibrosis

Punicalagin has myocardial protection; the mechanism of punicalagin on ventricular remodeling (VR) after acute myocardial infarction (AMI) remains unclear.. These studies explore the role and mechanism of punicalagin in preventing and treating VR after AMI.. Molecular docking was used to predict the targets of punicalagin. After 2 weeks of AMI model, the SD rats were randomly divided into model, and punicalagin (200, 400 mg/kg, gavage) groups for 4 weeks. Thoracotomy with perforation but no ligature was performed on rats in control group. The protein expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis speck-like protein (ASC), caspase-1, gasdermin D (GSDMD), and GSDMD-N, the mRNA expression of NLRP3, caspase-1, GSDMD, interleukin-1β (IL-1β) and IL-18 were evaluated.. Punicalagin had binding activities with NLRP3 (Vina score, -5.8), caspase-1 (Vina score, -6.7), and GSDMD (Vina score, -6.7). Punicalagin could improve cardiac function, alleviate cardiac pathological changes, minimize the excessive accumulation of collagen in the left ventricular myocardium (. Punicalagin may provide a useful treatment for the future myocardial protection.

Topics: Animals; Apoptosis; Caspase 1; Fibrosis; Hydrolyzable Tannins; Male; Molecular Docking Simulation; Myocardial Infarction; Myocytes, Cardiac; Rats; Rats, Sprague-Dawley; Signal Transduction; Ventricular Remodeling