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Vine tea (Ampelopsis grossedentata), a traditional Chinese tea, is rich in flavonoids with various biological activities. Our study found that Vine tea total flavonoids (TFs) treatment reduced the body mass and blood lipid levels and improved the hepatic tissue morphology in mice fed the high-fat diet (HFD). In vivo, TF treatment activated the hepatic adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, initiated autophagy, and regulated the expression levels of proteins for lipid metabolism in those HFD-fed mice. In vitro, TF treatment dramatically reduced the lipid droplets and triacylglycerol content in HepG2 and L02 cells treated with oleic acid (OA). These were associated with the activation of the AMPK/mTOR pathway and autophagy initiation in OA-treated hepatocytes. This phenotype was abolished in the presence of 3-methyladenine, an autophagy inhibitor. Our results indicated that the TF activation of AMPK/mTOR leads to the stimulation of autophagy and a decrease in the buildup of intracellular lipids in hepatocytes, showing the potential of TF as a therapeutic agent for nonalcoholic fatty liver disease. PRACTICAL APPLICATION: Vine tea, a tea drink, has been consumed by Chinese folk for over a thousand years. The result of this study will provide evidence that vine tea total flavonoids have potential use as a functional material for the prevention and amelioration of nonalcoholic fatty liver disease., (© 2024 Institute of Food Technologists.)

The corpus luteum is primarily responsible for the production and secretion of progesterone. Melatonin has been established to regulate autophagy and induce progesterone secretion in luteal cell. However, whether melatonin affects progesterone secretion by interfering with autophagy is yet to be reported. In the present study, the expression levels of melatonin receptors (MT1 and MT2), autophagy-related protein Beclin1 (Bec1), microtubule-associated protein light chain 3 B (LC3B), progesterone and steroidogenic acute regulatory protein (StAR), and cytochrome P450scc (CYP11A1) were analyzed in the corpus luteum of sheep at different stages (early, middle, and late); specifically, enzyme-linked immunosorbent assays, immunohistochemical staining, and western blotting were utilized for this expression analysis. In addition, to determine whether melatonin regulated progesterone secretion via the regulation of autophagy, luteal cells were cultured before being exposed to different concentrations of melatonin (0.01–100 nM) and the autophagy inhibitor chloroquine (50 μM). Next, luteal cells were treated with the melatonin receptor inhibitors 4-phenyl-2-propionamidotetralin (1 μM) and luzindole (1 μM) before detecting Bec1, LC3B2, AMPK/mTOR, and progesterone secretion levels to ascertain whether the effect of melatonin on autophagy and progesterone secretion is mediated by its corresponding receptors in luteal cells. Finally, to determine the significance of the AMPK/mTOR pathway in this process, an AMPK inhibitor, Compound C (10 μM), was added to luteal cells. Overall, the highest expression of melatonin receptors, autophagy and progesterone secretion was observed in the middle-phase corpus luteum; additionally, melatonin promoted autophagy, at least partially, through its receptor-mediated AMPK/mTOR pathway, which thereby promoting progesterone secretion in luteal cells in vitro. Ultimately, this study is the first to clarify the important role of autophagy in the melatonin-mediated regulation of progesterone secretion in the corpus luteum of sheep; it also lays a foundation for further exploration into the role of melatonin in regulating sheep's ovarian function. • The high level of melatonin receptors, autophagy and progesterone secretion were in the middle-phase corpus luteum. • Melatonin promoted luteal cell autophagy in sheep luteal cells. • Melatonin promoted sheep luteal cell progesterone secretion through its receptor-mediated autophagy. [ABSTRACT FROM AUTHOR]