Hypaphorine ameliorates lipid accumulation and inflammation in a cellular model of non alcoholic fatty liver by regulating p38/JNK and NF κB signaling pathways

Abstract

Purpose: To investigate the therapeutic effect and underlying mechanism of hypaphorine in a cellular model of non-alcoholic fatty liver disease (NAFLD).Methods: Palmitic acid (PA) was used to induce a NAFLD phenotype in hepatocytes. Cell viability and apoptosis were evaluated by CCK-8 and flow cytometry assays. Inflammatory response was measured by enzyme-linked immunosorbent assay (ELISA). The effect of hypaphorine on lipid accumulation was evaluated using Oil Red O staining and triglyceride kits. Activation of p38/c–Jun N-terminal kinase (JNK) and NF-κB pathways were analyzed by immunoblot assay.Results: Hypaphorine significantly improved cell viability (p < 0.01), suppressed inflammatory response (p < 0.01), and reduced lipid accumulation (p < 0.01) in PA-treated hepatocytes. Hypaphorine ameliorated lipid accumulation and inflammation in PA-treated hepatocytes by targeting p38/JNK and NF-κB pathways.Conclusion: Hypaphorine may serve as a therapeutic target in NAFLD. However, in vivo studies to validate this finding are required.