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