Study on the Mechanism and Protection of Salt-Sensitive Hypertensive Rats’ Myocardial Fibrosis by Regulating Striatin with Sacubatrovalsartan

Abstract

This study aims to explore the relationship between STRN, TGF-β1, Caspase-3, PD-1 expression, and myocardial fibrosis in salt-sensitive hypertensive rats. It investigates the correlation between STRN expression and myocardial fibrosis, along with the protective effects of Sacubitril/Valsartan (ARNI). Fifteen 18-week-old rats were divided into three groups: Control, high salt (SSH), and ARNI+SSH. Blood pressure was monitored weekly for 8 weeks. Echocardiography evaluated cardiac parameters, while H&E and Masson staining visualized myocardial morphology and fibrosis. Immunohistochemistry measured protein expression of collagen-1, collagen-3, TGF-β1, PD-1, Caspase-3, and STRN. Western blot assessed STRN protein levels. High-salt diet increased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3, and reduced STRN expression compared to Control (P < 0.05). ARNI treatment decreased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3 (P <0.05), and increased STRN expression compared to SSH (P <0.05). STRN expression correlated positively with myocardial fibrosis. ARNI demonstrated potential in attenuating fibrosis by modulating STRN expression and suppressing apoptosis and inflammation in salt-sensitive hypertensive rats.