sirolimus has been researched along with alpha-terpineol* in 1 studies
1 other study(ies) available for sirolimus and alpha-terpineol
Article | Year |
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α-Terpineol induces fatty liver in mice mediated by the AMP-activated kinase and sterol response element binding protein pathway.
The use of herbal medicines in disease prevention and treatment is growing rapidly worldwide, without careful consideration of safety issues. α-Terpineol is a monoterpene alcoholic component of Melaleuca alternifolia, Salvia officinalis and Carthamus tinctorius that is used widely as a flavor and essential oil in food. The present study showed that α-terpineol induces fatty liver via the AMP-activated protein kinase (AMPK)-mTOR-sterol regulatory element-binding protein-1 (SREBP-1) pathway. α-Terpineol-treated hepatocytes had significantly increased neutral lipid accumulation. α-Terpineol suppressed AMPK phosphorylation, and increased p70S6 kinase (p70S6K) phosphorylation and SREBP-1 activation. It also increased luciferase activity in cells transfected with LXRE-tk-Luc and SRE-tk-Luc. Inhibition of mTOR signaling by co-treatment with rapamycin or co-transfection with dominant negative p70S6K blocked completely the effects of α-terpineol. α-Terpineol oral administration to mice for 2weeks led to decreased AMPK phosphorylation and increased SREBP-1 activation in the liver, followed by hepatic lipid accumulation. Conversely, rapamycin co-treatment reversed α-terpineol-induced SREBP-1 activation and fatty liver in mice. These data provide evidence that α-terpineol causes fatty liver, an effect mediated by the AMPK/mTOR/SREBP-1 pathway. Topics: AMP-Activated Protein Kinases; Animals; Base Sequence; Cell Line, Tumor; Cyclohexane Monoterpenes; Cyclohexenes; DNA Primers; Fatty Liver; Humans; Male; Mice; Mice, Inbred C57BL; Monoterpenes; Phosphorylation; Sirolimus; Sterol Regulatory Element Binding Protein 1 | 2013 |