Folic acid reduced fatty liver injury in rat and HepG2 models, apparently through -linked .
Evidence
Preclinical rat and cell experiments used a high-fat-diet MAFLD rat model and palmitic-acid-treated HepG2 cells, measuring liver injury markers, lipids, inflammation, autophagy proteins, and NRF2 knockdown effects.
Caveat
The evidence comes from animal and HepG2 models, so it does not show clinical benefit for people with MAFLD.
Simplified
(MAFLD) is a liver disease characterized by hepatic steatosis and excessive accumulation of lipids, with a high global incidence, especially in populations with obesity, diabetes and metabolic syndrome (MetS). As an important B vitamin, folate (FA) is stored mainly in the liver where it regulates oxidative stress, chronic inflammation and lipid metabolism. However, its regulatory role and mechanism of action in MAFLD are still poorly understood. Therefore, this study was conducted to investigate the regulatory effect of FA on MAFLD. The MAFLD rat model was induced by a high-fat diet (HFD), and HepG2 cells were treated with 0.3 mM palmitic acid (PA) for 24 h to establish a cell model. The expression of relevant genes and proteins was detected by RT-qPCR and Western blotting. Injury to HepG2 cells and rat liver tissues was evaluated via hematoxylin and eosin staining, Oil red O staining, ELISA and CCK-8 assay. FA treatment inhibited body weight gain in rats and reduced the levels of liver injury indicators (aspartate and alanine aminotransferase, and Alkaline phosphatase), blood lipids (total cholesterol, triglycerides and free fatty acids) and inflammatory cytokines (TNF-α, IL-6, and IL-1β), reducing lipid accumulation and pathological damage in the liver and ultimately alleviating the progression of MAFLD. Moreover, FA treatment promoted the expression of the -related protein LC3 II/I, inhibited the expression of p62, and increased the formation of autophagosomes, thereby alleviating PA-induced damage to HepG2 cells. Furthermore, expression is downregulated in MAFLD and can be upregulated by FA treatment. Further examination revealed that knocking down NRF2 could partially attenuate the inhibitory effect of FA on PA-induced HepG2 cell injury. In conclusion, FA activates autophagy by promoting the expression of NRF2, thereby alleviating the development of MAFLD.
Key numbers
Not specified
Decrease in body weight gain
treatment reduced body weight gain in rats.
Not specified
Reduction in liver injury markers
treatment decreased serum AST and ALT levels in rats.
Not specified
Promotion of
treatment increased the expression of -related proteins in .
Full Text
We can’t show the full text here under this license.
