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

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-kappa B 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-kappa B pathways. Conclusion: Hypaphorine may serve as a therapeutic target in NAFLD. However, in vivo studies to validate this finding are required.