Salvianolic acid B mitigates metabolic dysfunction-associated steatohepatitis in mice via up-regulating SIRT1 to inhibit hepatocyte ferroptosis (APASL 2025) - Jan 4, 2025 - Abstract #PP0396; " In vivo, MASH models were induced by a high-fat and high-cholesterol (HFHC) diet for 30 consecutive weeks in C57/BL mice, and treated with Sal B, obeticholic acid (OCA) or a SIRT1 agonist, SRT1720 in the beginning of 24th week. In vitro, stable over-expression and knockdown of SIRT1 in hepatocytes were constructed with lentivirus, subsequently, a hepatocyte lipid deposition model induced by palmitic acid/oleic acid (PO) and a hepatocyte ferroptosis model induced by erastin were used to investigate the efficacy and mechanism of Sal B. Furthermore, the interaction and the binding kinetics of Sal B and SIRT1 were determined by molecular docking and molecular dynamics simulation, as well as DARTS, CESTA and SPR... The activation of SIRT1 inhibits hepatocyte ferroptosis and represents a novel therapeutic target for the treatment of MASH. Sal B ameliorates MASH in mice via regulating SIRT1/p53 signaling to inhibit hepatocyte ferroptosis, providing experimental data..."
Preclinical • Fibrosis • Hepatology • Immunology • Inflammation • Liver Cirrhosis • Metabolic Disorders • Metabolic Dysfunction-Associated Steatohepatitis
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Xiaoxi Zhou 1; Yadong Fu 1, 2; Jinxing Lv 1; Zheng Zhang 1; Yue Liang 1; Wei Liu 1; Jiamei Chen 1; Ping Liu 1, 3
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