Chaoyu Wei, Wei Zhou

For correspondence:-  Wei Zhou   Email: wzhou3137@163.com

Accepted: 28 November 2022        Published: 29 December 2022

Citation: Wei C, Zhou W. Hypaphorine ameliorates lipid accumulation and inflammation in a cellular model of non-alcoholic fatty liver by regulating p38/JNK and NF-κB signaling pathways. Trop J Pharm Res 2022; 21(12):2569-2574 doi: 10.4314/tjpr.v21i12.10

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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.