Abstract
Nonalcoholic fatty liver disease (NAFLD), which promotes serious health problems, is related to the increase in the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and pyroptosis by a high-fat diet (HFD). Whether dieckol (DK), a component of Ecklonia cava extracts (ECE), attenuated NAFLD in an HFD-induced NAFLD animal model was evaluated. The expression of high mobility group box 1/Toll-like receptor 4/nuclear factor-κB, which initiated the NLRP3 inflammasome, was increased in the liver of HFD-fed animals and significantly decreased with ECE or DK administration. The expression of NLRP3/ASC/caspase-1, which are components of the NLRP3 inflammasome, and the number of pyroptotic cells were increased by HFD and decreased with ECE or DK administration. The accumulation of triglycerides and free fatty acids in the liver was increased by HFD and decreased with ECE or DK administration. The histological NAFLD score was increased by HFD and decreased with ECE or DK administration. The expression of lipogenic genes (FASN, SREBP-2, PPARγ, and FABP4) increased and that of lipolytic genes (PPARα, CPT1A, ATGL, and HSL) was decreased by HFD and attenuated with ECE or DK administration. In conclusion, ECE or DK attenuated NAFLD by decreasing the NLRP3 inflammasome and pyroptosis.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is categorized by histology, pathogenesis, and natural history from isolated steatosis or nonalcoholic fatty liver to nonalcoholic steatohepatitis (NASH) [1]
Isolated steatosis is characterized by excess fat deposition without injury or inflammation; NASH is accompanied by hepatocyte ballooning, liver injury, inflammation, and varying degrees of fibrosis, eventually causing cirrhosis and acting as risk factors of end-stage liver disease and hepatocellular carcinoma [1]
The HMGB1 expression in the cytoplasm was significantly increased in the liver of the high-fat diet (HFD) group compared to in the normal fat diet (NFD) group and significantly decreased with either
Summary
Nonalcoholic fatty liver disease (NAFLD) is categorized by histology, pathogenesis, and natural history from isolated steatosis or nonalcoholic fatty liver to nonalcoholic steatohepatitis (NASH) [1]. Isolated steatosis is characterized by excess fat deposition without injury or inflammation; NASH is accompanied by hepatocyte ballooning, liver injury, inflammation, and varying degrees of fibrosis, eventually causing cirrhosis and acting as risk factors of end-stage liver disease and hepatocellular carcinoma [1]. NAFLD prevalence is predicted to be between 20% and 30% in the general population, but it is increasing by up to 75% in those with morbid obesity [2,3,4]. The definite etiology of NAFLD has not been fully revealed. Animal models fed with a high-fat diet (HFD) have shown histological changes and metabolic abnormalities of NAFLD [7,8,9]
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