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Luteolin prevents palmitic acid‐induced hepatic steatosis by regulating ER stress in HepG2
Author(s) -
Chei Sungwoo,
Hwang JiHyun,
Lee YeonJoo,
Koh EunJeong,
Choi Jia,
Song JiHyeon,
Seo YoungJin,
Choi SeoYun,
Park MinKi,
Lee BooYong
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.972.23
Subject(s) - palmitic acid , luteolin , steatosis , chemistry , apoptosis , tumor necrosis factor alpha , biochemistry , fatty acid , medicine , endocrinology , biology , antioxidant , flavonoid
Luteolin is a plant flavone and most often found leaves. In this study, we determine whether luteolin prevents palmitic acid‐induced hepatic steatosis by regulating ER stress in HepG2 cells, human hepatocyte cell line. To examine the effects of luteolin on palmitic acid‐induced hepatic steatosis, HepG2 cells were treated with low dose and high dose of luteolin in the presence or absence of palmitic acid. We indicated whether palmitic acid induced the hepatic steatosis in HepG2 cells. Palmitic acid increased lipid accumulation via stimulated SREBP protein level and phosphorylation of ACC. Also, palmitic acid‐stimulated HepG2 cells were observed apoptosis and necrosis. Using the in vitro model, we treated luteolin on palmitic acid‐stimulated HepG2. Luteolin reduced lipid accumulation and inhibited SREBP1 protein level and phosphorylation. Beside, luteolin treatment decreased apoptosis and necrosis via regulation of ER stress related factor (PERK and eIF2α) in palmitic acid‐stimulated cells. Furthermore, luteolin decreased secretion of inflammatory cytokines, such as interleukin and TNF, by inhibiting NF‐κB activation. Luteolin may inhibit the ER stress and the inflammatory responses on palmitic acid‐induced hepatic steatosis.