Gomisin J inhibits oleic acid-induced hepatic lipogenesis by activation of the AMPK dependent pathway and inhibition of the hepatokine fetuin-A in HepG2 cells
- Gomisin J inhibits oleic acid-induced hepatic lipogenesis by activation of the AMPK dependent pathway and inhibition of the hepatokine fetuin-A in HepG2 cells
- 김명석; 아흐마드 란디; 남의정; 노주원
- Gomisin J; AMPK; fetuin-A; HepG2; LKB1
- Issue Date
- The 6th International Conference on Food Factors
- The aim of our study is to investigate the molecular mechanism of gomisin J from Schisandra
chinensis on the oleic acid (OA)-induced lipid accumulation in HepG2 cells. Triglyceride (TG) assays, and Oil red O staining were used to determine lipid accumulation in the HepG2 cells. Gomisin J attenuated lipid accumulation in OA-induced HepG2 cells. It also suppressed the expression of lipogenic enzymes and inflammatory mediators and increased the expression of lipolytic enzymes in OA-induced HepG2 cells. Furthermore, the use of specific inhibitors and fetuin-A-siRNA and liver kinase B1 (LKB1)-siRNA transfected cells demonstrated that gomisin J regulated lipogenesis and lipolysis via inhibition of fetuin-A and activation of an AMP-activated protein kinase (AMPK)-dependent pathway in HepG2 cells. Our results showed that gomisin J suppressed lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1, and Ca2+/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. It suggested that gomisin J has potential benefits in preventing and treating nonalcoholic fatty liver disease.
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