Sericin Peptide Attenuates Non-Alcoholic Steatohepatitis Via Mitochondrial Function Modulation

Abstract

Sericin is a component of cocoons. Studies have shown that sericin improves metabolic disease in animal model. However, it is not yet known whether sericin is effective in the treatment of non-alcoholic steatohepatitis. Twenty C57BL/6N mice were divided into control and sericin treated group. High fat diet was fed to mice for 10 weeks. From 11th to 21st week sericin and distilled water were administered assigned groups via oral gavage. Body weight and liver to body weight ratio was assessed. AST, ALT, triglyceride, cholesterol and blood glucose levels were measured. qRT-PCR, Electro-microscopy, and Free fatty acid induced lipotoxicity assay were performed. Mitochondrial membrane potential was checked. As a result, there were no differences in body weight and diet intake in two groups. However, liver weight and liver/body weight ratio were significantly decreased in sericin group than in control group. Both the degree of hepatic steatosis and inflammation were lower in sericin group than the control group. NAFLD activity score were also decreased in treatment group. Serum ALT, AST, and triglyceride levels as well as area under receiver operating characteristics of oral glucose tolerance test were significantly decreased in sericin group. Hepatic mRNA expressions of TNF-α, MCP-1, and IL-6 mRNA were decreased in sericin group. Electron microscopy findings showed restoration of abnormal mitochondria with sericin treatment. Lipotoxicity induced HepG2 cell death was significantly attenuated in palmitic acid and sericin co-treated cells. Sericin also prevented palmitic acid induced mitochondrial depolarization. In conclusion, Sericin peptide treatment attenuated non-alcoholic steatohepatitis via mitochondrial function modulation.