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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Sci+Rep
2016 ; 6
(ä): 24399
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A pharmacological inhibitor of NLRP3 inflammasome prevents non-alcoholic fatty
liver disease in a mouse model induced by high fat diet
#MMPMID27075683
Yang G
; Lee HE
; Lee JY
Sci Rep
2016[Apr]; 6
(ä): 24399
PMID27075683
show ga
The activation of NOD-like receptor family pyrin domain containing 3 (NLRP3)
inflammasome is closely associated with the development and progression of
non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet. Therefore,
we investigated whether oral administration of sulforaphane (SFN) prevented
high-fat diet-induced NAFLD in mice by regulation of the NLRP3 inflammasome in
the liver. Daily oral administrations of SFN reduced hepatic steatosis scores,
serum ALT and AST levels, and hepatic levels of cholesterol, triglycerides, and
free fatty acids in mice fed a high-fat diet. These were correlated with the
suppression of NLRP3 inflammasome activation in the liver by SFN as evidenced by
decrease in mRNA levels of ASC and caspase-1, caspase-1 enzyme activity, and
IL-1? levels. SFN inhibited saturated fatty acid-induced activation of the NLRP3
inflammasome in primary mouse hepatocytes, accompanied by the restoration of
mitochondrial dysfunction. The suppression of NLRP3 inflammasome by SFN was
mediated by the regulation of AMP-activated protein kinase-autophagy axis. Our
findings demonstrated that the suppression of NLRP3 inflammasome activation by an
orally available small molecule inhibitor leads to the alleviation of the hepatic
steatosis symptoms associated with NAFLD induced by a high-fat diet.