Codonopsis pilosula polysaccharides attenuate lipid accumulation and inflammatory response in the NAFLD mouse by regulating AMPK/ACC/SREBP1 signaling pathway

This study investigated the effects of Codonopsis pilosula Polysaccharides (CPP) on nonalcoholic fatty liver disease (NAFLD) induced by a high-fat diet in mice and its underlying mechanisms. Mice were divided into six groups: control, model, fenofibrate, and three CPP dosage groups (300, 200, 100 mg/kg). CPP reduced liver lipid accumulation, serum TC, TG, LDL-C, ALT, AST, MDA, IL-6, and TNF-α levels while increasing HDL-C, SOD, and GSH-Px levels (P < 0.05). Histopathological analysis confirmed decreased lipid deposition. Western blot showed CPP enhanced AMPK and ACC phosphorylation, while RT-PCR revealed reduced expression of SREBP1 and its target genes. In PA-induced HepG2 cells, CPP effects were reversed by AMPK inhibition. These findings demonstrate CPP's potential to mitigate hepatocellular lipotoxicity, oxidative stress, and inflammation in NAFLD through the AMPK/ACC/SREBP1 pathway, offering a promising therapeutic approach.

AMPK/ACC/SREBP1 signaling pathway; Codonopsis pilosula polysaccharide; Inflammatory factors; Nonalcoholic fatty liverdisease; Oxidative stress.