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Diets rich in fat are a major cause of metabolic disease, and nutritional food has been widely used to counteract the metabolic disorders such as obesity and fatty liver. The present study investigated the effects of oleuropein-enriched extract from Jasminum grandiflorum L. flowers (OLE-JGF) in high-fat diet (HFD)-fed mice and oleic acid (OA)-treated AML-12 cells. Treatment of HFD-fed mice with 0.6% OLE-JGF for 8 weeks significantly reduced body and liver weights, as well as attenuating lipid dysmetabolism and hepatic steatosis. OLE-JGF administration prominently suppressed the mRNA expressions of monocyte chemoattractant protein-1 (MCP-1) and cluster of differentiation 68 (CD68), and it also downregulated acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) as well as sterol-regulatory-element-binding protein (SREBP-1c) in the liver. Meanwhile, mitochondrial DNA and uncoupling protein 2 (UCP2) were upregulated along with the increased expression of mitochondrial biogenic promoters including liver kinase B1 (LKB1), peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α), nuclear factor-erythroid-derived 2-like 2 (Nrf2), and mitochondrial transcription factor A (Tfam), but did not change AMP-activated protein kinase (AMPK) in liver. The lipid droplets were decreased significantly after treatment with 80 μM oleuropein for 24 h in OA-induced AML-12 cells. Furthermore, oleuropein significantly inhibited ACC mRNA expression and upregulated LKB1, PGC-1α, and Tfam mRNA levels, as well as increasing the binding level of LKB1 to PGC-1α promoter in OA-induced cells. These findings indicate that OLE-JGF reduces hepatic lipid deposition in HFD-fed mice, as well as the fact that OA-induced liver cells may be partly attributed to upregulation of the LKB1-PGC-1α axis, which mediates hepatic lipogenesis and mitochondrial biogenesis. Our study provides a scientific basis for the benefits and potential use of the J. grandiflorum flower as a food supplement for the prevention and treatment of metabolic disease. [ABSTRACT FROM AUTHOR]

The lipid-lowering effects of a water extract of Jasminum grandiflorum L. (WE) and its chemical components on 3T3-L1 preadipocytes was investigated. To determine the inhibitory effects of J. grandiflorum samples on lipid droplet development, oil red O staining was used to quantify and detect triglyceride (TG) contents following the induction of 3T3-L1 preadipocytes to produce mature adipocytes. Liquid chromatography-mass spectrometry was used to analyze the chemical components in the water extract of J. grandiflorum, an MTT assay was used to determine the effects of J. grandiflorum and its components on the proliferation of 3T3-L1 preadipocytes, and western blotting was performed to determine the expression of AMPK, C/EBPα, FAS, ACC, CPT1, Bax, and Bcl-2 proteins. The results revealed that the WE can significantly inhibit the formation of lipid droplets in a dose-dependent manner. A high concentration of WE (500 µg/mL) was found to reduce the contents of neutral lipids and TG by 23.59% and 30.20%, respectively. These effects were found to be most significant during the early stage of fat accumulation, and it was established that the active constituent contributing most to this lipid-lowering effect was oleuropein, with a content of 13.77%. Furthermore, WE and oleuropein were shown to activate the phosphorylation of AMPK (123.19% and 115.98%, respectively) and its downstream target ACC (451.06% and 1 050.0%), and to downregulate the protein expression of its downstream target FAS (81.72% and 60.50%). This had the effect of reducing adipogenesis and increasing the expression of CPT1 (164.84% and 292.19%), and accelerating fatty acid oxidation. Moreover, it inhibited the expression of C/EBPα (68.97% and 34.57%), thereby affecting the differentiation of 3T3-L1 cells, and also upregulated the expression of Bax (154.60% and 139.37%) and downregulated the expression of Bcl-2 (41.10% and 45.62%), thus inducing 3T3-L1 cell apoptosis. These findings indicate that a WE of J. grandiflorum can inhibit cell growth, differentiation, and lipid synthesis, and promote fatty acid oxidation during the early stage of 3T3-L1 cell differentiation, thereby effectively inhibiting lipid accumulation, the underlying mechanism of which may involve the regulation of AMPK and Bax/Bcl-2 pathways. [ABSTRACT FROM AUTHOR]

Four novel stemphol derivatives, pleosporols A–D (1, 2 and mixture of 3 and 4) together with known compounds stemfolones (mixture of 5 and 6), stemphol (7) were isolated from a marine fungus Pleospora sp. (PO4) derived from the gut of marine isopod Ligia oceanica. The planar structures of novel compounds were elucidated on the basis of mass and NMR spectral analysis. The stereo-chemistries of 1–2 were determined by CD spectra, NOESY data, coupling constants analysis and modified Mosher's method while the absolute configurations of 3–6 were not clear. Novel compounds contained α, β-unsaturated cyclohexanone ring and possibly derived from the oxidation of stemphol. All novel ones showed strong antimicrobial activity against Staphylococcus epidermidis CMCC26069 with MIC values less than 10 μg/mL. [ABSTRACT FROM AUTHOR]