Key result
Gardenoside significantly decreased FFA-induced cellular steatosis in HepG2 cells without cytotoxicity, and suppressed inflammatory cytokine production and intracellular NFκB activity.
Why the study?
Does Gardenoside reduce cellular steatosis and inflammation in FFA-induced HepG2 hepatocytes?
Does Gardenoside reduce cellular steatosis and inflammation in FFA-induced HepG2 hepatocytes?
Gardenoside protects against FFA-induced cellular steatosis and inflammation in HepG2 cells, suggesting potential therapeutic value for non-alcoholic steatohepatitis (NASH).
May merit in vivo validation for NASH; leaves open clinical translation pending human data.
Gardenoside is one of the most important effective extractions of a herb for its hepatoprotective properties. The aim of this study was to address the mechanism of Gardenoside on HepG2 cellular steatosis induced by free fatty acids (FFAs). The model of HepG2 steatosis was duplicated by oleic and palmitic acid at the proportion of 2:1 (FFAs mixture) for 24 h, then lipid toxicity was induced. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) were used to detect cell viability and Oil Red O staining method was used to judge the lipid accumulation respectively. Inflammatory cytokines TNF-α, IL-1β, IL-6 and intracellular NFκB were measured after 24 h. The steatosis was significantly decreased after Gardenoside treatment without cytotoxicity. TNF-α, IL-1β, IL-6 were modulated to HepG2 cells by treatment of Gardenoside. In the meantime, the activation of NFκB was inhibited by Gardenoside. Gardenoside has a protective effect on FFA-induced cellular steatosis in HepG2 cells which indicates that Gardenoside might be a potential therapeutic herb against NASH by suppressed supernatant inflammatory cytokine production and intracellular NFkB activity.
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Liang et al. (2015) studied HepG2 cellular steatosis induced by free fatty acids. Gardenoside was evaluated on Cellular steatosis, cell viability, inflammatory cytokines, and intracellular NFκB. Gardenoside significantly decreased FFA-induced cellular steatosis in HepG2 cells without cytotoxicity, and suppressed inflammatory cytokine production and intracellular NFκB activity.
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