Sesamol ameliorates hepatic lipid accumulation and oxidative stress in steatosis HepG2 cells via the PPAR signaling pathway.
Longkai ShiEmad KarrarXingguo WangPublished in: Journal of food biochemistry (2021)
Non-alcoholic fatty liver disease (NAFLD) is a chronic hepatopathy caused by disordered lipid metabolism in the liver. Sesamol, a phenolic compound derived from sesame oil, has been shown to inhibit obesity, hyperlipidemia, and atherosclerosis in previous investigations. However, the preventive effect of sesamol against hepatic steatosis and oxidative stress in NAFLD has not been well-studied. In this work, sesamol was observed to alleviate lipid accumulation and oxidative stress in high oleic acid (300 μM)/cholesterol (25 μM) induced HepG2 cells, thus indicating that sesamol was involved in regulating hepatic lipid metabolism and oxidative injury. Mechanism studies found that the activated peroxisome proliferator-activated receptors (PPAR) signaling pathway by sesamol intervention up-regulated gene and protein expressions related to fatty acid oxidation and cholesterol efflux and catabolism, thus accelerating lipid consumption and reducing intracellular lipid accumulation in the process of NAFLD. These data suggested that sesamol can effectively ameliorate hepatic steatosis and sesamol riched sesamol oil may be a potential agent for finding therapeutic strategies to treat the NAFLD. PRACTICAL APPLICATIONS: Sesamol and sesamol-rich sesame oil have received much attention due to their performance on hepatic lipid regulation. The results of this study indicate that sesamol treatment could ameliorate hepatic steatosis by inhibiting lipid accumulation and oxidative stress, thus demonstrating that sesamol and sesame oil can be used for functional foods and nutraceutical applications in the future. In addition, the present work provides knowledge of the effects of sesamol on NAFLD and involved mechanisms, and further supplies nutritional guidelines for sesame oil consumption.
Keyphrases
- fatty acid
- oxidative stress
- signaling pathway
- diabetic rats
- insulin resistance
- dna damage
- healthcare
- randomized controlled trial
- type diabetes
- induced apoptosis
- pi k akt
- cardiovascular disease
- dna methylation
- weight loss
- adipose tissue
- binding protein
- physical activity
- small molecule
- machine learning
- body mass index
- electronic health record
- drug induced
- risk assessment
- high fat diet induced
- combination therapy
- endothelial cells
- liver fibrosis
- solid state