Effect of chlorogenic acid on LPS-induced proinflammatory signaling in hepatic stellate cells

Shi, Haitao; Dong, Lei; Dang, Xiaoyan; Liu, Yaping; Jiang, Jiong; Wang, Yan; Lu, Xiaolan; Guo, Xiaoyan

doi:10.1007/s00011-013-0610-7

Cited by 79 publications

(44 citation statements)

References 38 publications

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“…Glutathione is synthesized in tissues and cells (e.g., liver and intestine) from glutamate, cysteine and glycine, and hepatocytes are the major producer and exporter of glutathione (Wu et al 2004, Wu 2010). This finding is consistent with other studies in which CGA exerts a potent anti-oxidant effect in several animal models hepatic injury induced by CCl 4 , lipopolysaccharide, or acetaminophen (Ji et al 2013; Shi et al 2009, 2013; Xu et al 2010). In the present study, CGA supplementation increased hepatic concentrations of glutathione, indicating that CGA can promote glutathione synthesis in the liver.…”

Section: Discussionsupporting

confidence: 93%

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

et al. 2014

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This study was conducted to investigate effects of chlorogenic acid (CGA) supplementation on serum and hepatic metabolomes in rats. Rats received daily intragastric administration of either CGA (60 mg/kg body weight) or distilled water (control) for 4 weeks. Growth performance, serum biochemical profiles, and hepatic morphology were measured. Additionally, serum and liver tissue extracts were analyzed for metabolomes by high-resolution 1H nuclear magnetic resonance-based metabolomics and multivariate statistics. CGA did not affect rat growth performance, serum biochemical profiles, or hepatic morphology. However, supplementation with CGA decreased serum concentrations of lactate, pyruvate, succinate, citrate, β-hydroxybutyrate and acetoacetate, while increasing serum concentrations of glycine and hepatic concentrations of glutathione. These results suggest that CGA supplementation results in perturbation of energy and amino acid metabolism in rats. We suggest that glycine and glutathione in serum may be useful biomarkers for biological properties of CGA on nitrogen metabolism in vivo.

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Section: Discussionsupporting

confidence: 93%

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

et al. 2014

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“…Treatment with CGA significantly reduced the serum concentration of proinflammatory cytokines closely related with the development and progress of atherosclerosis such as IL-6, IL-8, TNFα and MCP-1 [39] (Figure 3) in ApoE −/− mice and decreased the intracellular levels of IL-1β, IL-6 and TNFα in LPS-elicited RAW264.7 cells (Figure 4), indicating a potent antiinflammatory activity as previously reported [31], [40]. In contrast, atorvastatin showed non-significant effect on serum IL-6, IL-8 and TNFα (Figure 3).…”

Section: Discussionsupporting

confidence: 78%

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

Luan

Zhang

et al. 2014

PLoS ONE

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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 in vivo effect of CGA.

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“…CHAs exhibit a broad range of biological activities: antibacterial, antifungal, hepatoprotective, antithrombotic, antiinflammatory and antioxidant activities [3][4][5][6][7][8]. Antioxidant activity of CHAs decrease the risk of several oxidative stress-related diseases, including atherosclerosis, some kinds of cancer and Alzheimer's disease [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Green and roasted coffee extracts as antioxidants in βTC3 cells with induced oxidative stress and lipid accumulation inhibitors in 3T3L1 cells, and their bioactivity in rats fed high fat diet

Budryn

Zakłos‐Szyda

Zaczyńska

et al. 2017

Eur Food Res Technol

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Effect of chlorogenic acid on LPS-induced proinflammatory signaling in hepatic stellate cells

Abstract: Our results indicate that CGA can efficiently inhibit LPS-induced proinflammatory responses in HSCs and the anti-inflammatory effect may be due to the inhibition of LPS/ROS/NF-κB signaling pathway.

Cited by 79 publications

References 38 publications

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

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

Green and roasted coffee extracts as antioxidants in βTC3 cells with induced oxidative stress and lipid accumulation inhibitors in 3T3L1 cells, and their bioactivity in rats fed high fat diet

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