@Article{ecn.2019.0437,
AUTHOR = {Sara Youssry, Maher A. Kamel},
TITLE = {Effect of folate supplementation on immunological and autophagy markers in experimental nonalcoholic fatty liver disease},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {4},
PAGES = {135--143},
URL = {http://www.techscience.com/ECN/v30n4/65384},
ISSN = {1952-4005},
ABSTRACT = {Background and aims: Chronic hepatic inflammation is an important pathogenic mediator of
nonalcoholic fatty liver disease (NAFLD) that contributes to disease severity. It is commonly suggested that autophagy
dysfunction may be an underlying cause of nonalcoholic fatty liver disease. However, the exact role of autophagy in lipid
metabolism remains controversial. There has been a growing interest in the role of folate supplementation for the
treatment and/or prevention of NAFLD. We aimed in this study to investigate the effects of different doses of folate
supplementation on several immune markers and autophagy trying to explore the complex role of IL-22 and autophagy
in NAFLD. Methods: Fifty Wistar rats were randomly separated into experimental (n = 40) and control groups
(n = 10), which were fed for eight weeks with a high-fat diet (HFD) containing 40% fats or a standard diet, respectively.
The experimental group was further subdivided into four subgroups where the first subgroup was left untreated while the
other three were treated with different doses of folate (50, 100, and 150 μg/kg of body weight, respectively). At the end
of the experimental period, animals from each group were sacrificed for blood and tissue analyses. Results: NAFLD rats
showed decreased IL-22 serum levels and increased LC3B expression as compared to controls. Folate treatment was
significantly associated with improvement in disease parameters, reduced presence of the pro-inflammatory cytokines
TNF-α and CXCL8 and LC3B expression, and increased IL-22 levels in a dose-dependent manner. Conclusion: These
results highlight the capacity of folate to modulate the production of several pro-inflammatory cytokines and autophagy
thereby having a favorable impact disease progression.},
DOI = {10.1684/ecn.2019.0437}
}