Chlorogenic acid (CGA) upregulates the transcriptional expression of PPARγ, LXRα, ABCA1 and ABCG1 in RAW264.7 cells.

<p>Real-time PCR was conducted with gene specific oligonucleotide primers. The amplification of β-actin served as the internal control. Values are means ± SEM of at least three experiments. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 vs. control.</p

Chlorogenic acid (CGA) inhibits oxidized low-density lipoprotein (oxLDL)-elicited foam cell formation in RAW264.7 cells.

<p>RAW264.7 cells were elicited by oxLDL for 24 h with or without supplementation of CGA or atorvastatin. Cells were then stained with Oil red O, and the representative staining pictures (A), the aborptance at 358 nm (B), and intracellular totale cholesterol content (C) were acquired. Bar  =  50 µm. Values are means ± SEM of at least three experiments. ^###<i>p</i><0.001 oxLDL group vs. blank group; *<i>p</i><0.05, **<i>p</i><0.01 test group vs. oxLDL group. Atorv.  =  atorvastatin, CGA  =  Chlorogenic acid,</p

Chartarlactams A–P, Phenylspirodrimanes from the Sponge-Associated Fungus <i>Stachybotrys chartarum</i> with Antihyperlipidemic Activities

Chemical examination of the solid culture of the endophytic fungus <i>Stachybotrys chartarum</i> isolated from the sponge <i>Niphates recondita</i> resulted in the isolation of 16 new phenylspirodrimanes, named chartarlactams A–P (<b>1</b>–<b>16</b>), together with eight known analogues. Their structures were determined on the basis of extensive spectroscopic analysis, including X-ray single-crystal diffraction for the determination of the absolute configurations. The isoindolone-drimane dimer chartarlactam L (<b>12</b>) was determined as a new skeleton. Compounds <b>1</b>–<b>6</b> and <b>8</b>–<b>24</b> were evaluated for antihyperlipidemic effects in HepG2 cells, and the primary structure–activity relationships are discussed

Chlorogenic Acid Protects against Atherosclerosis in ApoE^−/− Mice and Promotes Cholesterol Efflux from RAW264.7 Macrophages

<div><p>Chlorogenic acid (CGA) is one of the most abundant polyphenols in the human diet and is suggested to be a potential antiatherosclerotic agent due to its proposed hypolipidemic, anti-inflammatory and antioxidative properties. The aim of this study was to evaluate the effect of CGA on atherosclerosis development in ApoE^−/− mice and its potential mechanism. ApoE^−/− mice were fed a cholesterol-rich diet without (control) or with CGA (200 and 400 mg/kg) or atorvastatin (4 mg/kg) for 12 weeks. During the study plasma lipid and inflammatory parameters were determined. Treatment with CGA (400 mg/kg) reduced atherosclerotic lesion area and vascular dilatation in the aortic root, comparable to atorvastatin. CGA (400 mg/kg) also significantly decreased plasma levels of total cholesterol, triglycerides and low-density lipoprotein-cholesterol as well as inflammatory markers. Supplementation with CGA or CGA metabolites-containing serum suppressed oxidized low-density lipoprotein (oxLDL)-induced lipid accumulation and stimulated cholesterol efflux from RAW264.7 cells. CGA significantly increased the mRNA levels of PPARγ, LXRα, ABCA1 and ABCG1 as well as the transcriptional activity of PPARγ. Cholesterol efflux assay showed that three major metabolites, caffeic, ferulic and gallic acids, significantly stimulated cholesterol efflux from RAW264.7 cells. These results suggest that CGA potently reduces atherosclerosis development in ApoE^−/− mice and promotes cholesterol efflux from RAW264.7 macrophages. Caffeic, ferulic and gallic acids may be the potential active compounds accounting for the <i>in vivo</i> effect of CGA.</p></div

Chlorogenic acid (CGA) metabolites-containing serum from CGA-treated normal mice decreases lipid accumulation and stimulates cholesterol efflux from RAW264.7 cells.

<p>Normal C57BL/6J mice were orally gavaged with 400 mg/kg of CGA or equal volume of distilled water for 3 days and blood was collected at 45 min after the final treatment. 1% (v/v) of serum from CGA-treated normal mice (S_CGA) significantly decreased oxLDL-induced neutral lipid accumulation (A) and total cholesterol (B), and stimulates cholesterol efflux (C) in RAW264.7 cells as compared with that from distilled water-treated animals (S_NC). Values are means ± SEM of at least three experiments. **<i>p</i><0.01, ***<i>p</i><0.001.</p

The serum lipid profile.

<p>TC: total cholesterol; TG: triglyceride; HDL-c: high-density lipoprotein-cholesterol; LDL-c; low-density lipoprotein-cholesterol; Atorva: atorvastatin; CGA: chlorogenic acid.</p><p>^*<i>p</i><0.05.</p><p>^**<i>p</i><0.01 v.s. ApoE.</p>−/−<p>mice (n = 6).</p><p>The serum lipid profile.</p

Chlorogenic acid (CGA) increases the transcriptional activity of PPARγ.

<p>The transcriptional activity of PPARγ was assessed by transactivation reporter assay in 293T cells. Rosiglitazone (5 µM) was used as positive control. Values are means ± SEM of at least three experiments. *<i>p</i><0.05, **<i>p</i><0.01 vs. control. Rosigli  =  rosiglitazone, CGA  =  Chlorogenic acid.</p

Primers used in quantitative real-time reverse transcription-PCR.

Primers used in quantitative real-time reverse transcription-PCR.</p

Effects of SH on the mRNA levels of genes in NLRP3-ASC3-caspase-1 pathway.

Data are shown as means ± sem. *PP<0.01.</p

Treatment with chlorogenic acid (CGA) reduces intracellular levels of IL-1β (A), IL-6 (B) and TNFα (C) elicited by LPS in RAW264.7 cells.

<p>Values are means ± SEM of at least three experiments. ^###<i>p</i><0.001 LPS+vehicle group vs. vehicle group; *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 test group vs. LPS+vehicle group. Atorv.  =  atorvastatin, CGA  =  Chlorogenic acid, LPS  =  lipopolysaccharides.</p