Zeaxanthin prevents ferroptosis by promoting mitochondrial function and inhibiting the p53 pathway in free fatty acid-induced HepG2 cells
In this study, free fatty acid (FFA) induced HepG2 cells were used as a cell model for NAFLD. Our results suggest that ZEA exerts antioxidative and anti-inflammatory effects in FFA-induced HepG2 cells. Moreover, ZEA acted as a ferroptosis inhibitor, significantly reducing reactive oxygen species (ROS) generation and iron overload and improving mitochondrial dysfunction in FFA-induced HepG2 cells. In addition, ZEA downregulated the expression of p53 and modulated downstream targets, such as GPX4, SLC7A11, SAT1, and ALOX15, which contributed to the reduction in cellular lipid peroxidation. Our findings suggest that ZEA has the potential for NAFLD intervention.PMID:36690321 | DOI:10.1016/j.bbalip.2023.159287
Source: Biochimica et Biophysica Acta - Category: Biochemistry Authors: Huimin Liu Jie Yan Fengtao Guan Zhibo Jin Jiahan Xie Chongrui Wang Meihong Liu Jingsheng Liu Source Type: research
More News: Age-Related Macular Degeneration (AMD) | Alcoholism | Biochemistry | Diabetes | Eating Disorders & Weight Management | Endocrinology | Fatty Liver Disease (FLD) | Iron | Liver | Liver Disease | Mitochondrial Disease | Non-alcoholic Fatty Liver Diseases (NAFLD) | Obesity | Study | Urology & Nephrology | Zeaxanthin