The açaí flavonoid velutin is a potent anti-inflammatory agent: blockade of LPS-mediated TNF-α and IL-6 production through inhibiting NF-κB activation and MAPK pathway

Xie, Cheng-Hui; Kang, Jie; Li, Zhimin; Schauss, Alexander G.; Badger, Thomas M.; Nagarajan, Shanmugam; Wu, Tong; Wu, Xianli

doi:10.1016/j.jnutbio.2011.06.013

Cited by 175 publications

(117 citation statements)

References 37 publications

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“…In the present study, the secretion of TNF-α, IL-1β, IL-6, IL-12 and hBD-2 in gastric cancer cells were significantly increased, particularly following LPS treatment. This finding is consistent with that of a previous study (27).…”

Section: Discussionsupporting

confidence: 94%

CD14 knockdown reduces lipopolysaccharide-induced cell viability and expression of inflammation-associated genes in gastric cancer cells in vitro and in nude mouse xenografts

Zhang

Nie

et al. 2015

Molecular Medicine Reports

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Abstract. The present study examined the role of CD14 in the regulation of lipopolysaccharide (LPS)-induced effects on gastric cancer cells. MGC-803 cells were stably transfected with CD14 short hairpin (sh)RNA and treated with LPS, followed by assessment of cell proliferation, apoptosis and gene expression using a cell counting kit-8 assay, flow cytometry, reverse transcription-polymerase chain reaction and western blot analysis, respectively. The cells subjected to CD14 knockdown were treated with 10 g/ml LPS and injected into nude mice to form tumor xenografts. CD14 shRNA-transfected MGC-803 cells did not exhibit any significant changes in cell viability compared with the control cells (P>0.05), but cell viability was markedly increased in the wild-type (WT) + LPS group (P<0.05). In contrast to the WT + LPS group, the cell viability of the sh-CD14 + LPS group was markedly decreased (P<0.05). In addition, compared with those in the controls, the level of sh-CD14 cell apoptosis did not change significantly; however, it was markedly reduced in the LPS group. Compared with that in the WT + LPS group, the rate of apoptosis in the sh-CD14 + LPS group increased to a certain extent, while it remained lower in the control group. In addition, compared with that in the control, the expression of tumor necrosis factor-α, interleukin (IL)-1, IL-6 and IL-12, and human β-defensin 2 was significantly increased in the WT + LPS group, while, compared with that in the WT + LPS group, the expression of these genes was markedly reduced in the sh-CD14 + LPS group (P<0.05). The nude mouse experiments further confirmed the in vitro data, including the finding that LPS promoted the growth of xenografts, but knockdown of CD14 expression reduced the response of tumor cells to LPS treatment. In conclusion, LPS induced cell viability and the release of inflammatory cytokines, but inhibited gastric cancer cell apoptosis. Knockdown of CD14 expression had no significant effect on gastric cancer malignancy, but mediated LPS signal transduction. IntroductionGastric cancer is one of the most common types of cancer globally and accounted for 989,600 ovel cases and 738,000 cancer-associated fatalities in 2008 (1). >70% of novel gastric cancer cases and fatalities occur in the developing countries, while they have declined in the majority of developed countries, including countries in North America and Europe in previous decades (1). The risk factors for gastric cancer include Helicobacter (H.) pylori infection, history of tobacco smoking, and consumption of smoked foods, salted meat or fish and pickled vegetables. However, intake of fresh fruits and vegetables appears to lower the risk of gastric cancer (1). Regional variations in gastric cancer prevalence reflect the differences in dietary patterns and the prevalence of H. pylori infection (2). H. pylori is an aerobic Gram-negative bacterium found in the stomach, which causes chronic gastritis, peptic ulcers and gastric cancer. Thus, H. pylori infection has been classified as a class I carcinog...

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Section: Discussionsupporting

confidence: 94%

CD14 knockdown reduces lipopolysaccharide-induced cell viability and expression of inflammation-associated genes in gastric cancer cells in vitro and in nude mouse xenografts

Zhang

Nie

et al. 2015

Molecular Medicine Reports

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“…The TNF-Į biosynthesis could be regulated not only by NF-țB pathway but also by p38 MAPK (Xie et al, 2012) and JNK (Kang et al, 2010). Noteworthy, we have previously found that Cy inhibited p38 MAPK and JNK activation, indicating that both NF-țB and MAPK could be involved in the inhibition of LPS-induced TNF-Į production by Cy extract.…”

Section: Discussionmentioning

confidence: 76%

Anti-inflammatory activity of Cymbopogon citratus leaves infusion via proteasome and nuclear factor-κB pathway inhibition: Contribution of chlorogenic acid

Francisco

Costa

Figueirinha

et al. 2013

Journal of Ethnopharmacology

112

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inflammatory activity of Cymbopogon citratus leaves infusion via proteasome and nuclear factor-κB pathway inhibition: contribution of chlorogenic acid, Journal of Ethnopharmacology, http://dx.doi.org/10. 1016/j.jep.2013.03.077 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Activation of nuclear factor-țB, a master regulator of inflammation, was investigated by Western blot and gene reporter assay. Proteasome activity was assessed using a fluorogenic peptide.Results: Cymbopogon citratus extract and its polyphenols inhibited the cytokine production on human macrophages. This supports the anti-inflammatory activity of Cy polyphenols in physiologically relevant cells. Concerning the effect on the activation of nuclear factor (NF)-țB pathway, the results pointed to an inhibition of LPS-induced NF-țB activation by Cy and PFs.Chlorogenic acid was identified, by HPLC/PDA/ESI-MS n , as the main phenolic acid of the Cy infusion, and it demonstrated to be, at least in part, responsible by that effect. Additionally, it was verified for the first time, that Cy and PFs inhibited the proteasome activity, a complex that controls NF-țB activation, having CGA a strong contribution. Conclusions:The results evidenced, for the first time, the anti-inflammatory properties of Cymbopogon citratus through proteasome inhibition and, consequently NF-țB pathway and cytokine expression. Additionally, Cy polyphenols, in particular chlorogenic acid, were highlighted as bio-active compounds.

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“…Xie et al, (2012) showed that compounds in Aç ai such as flavonoids, particularly velutin, a unique flavone isolated from the pulp of Aç aí fruit, effectively inhibited the expression of TNF-α and IL-6 by inhibiting nuclear factor-κB activation and p38 and JNK phosphorylation. They also found lower serum levels of TNF-α and IL-6 in apo E-deficient mice fed with 5% freeze-dried Aç ai juice powder for 20 weeks.…”

Section: Journal Of Biology and Life Sciencementioning

confidence: 99%

Protective Effects of Açai in Combination with Vitamin C against Aluminum-Induced Toxicity in Rat Liver

Ahmed

Hamaad²

2017

JBLS

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Aluminum is associated with the pathogenesis of several diseases. Aç ai has recently emerged as a natural source of antioxidants. The present study was conducted to evaluate the protective effect of Aç ai in combination with vitamin C against the aluminum chloride induced toxicity. Seventy rats were divided into 7 groups:-Group (GP) 1: control group, GP 2: treated with AlCl3, GP 3: treated with Aç ai, GP 4: treated with vitamin C, GP 5: treated with AlCl3 and Aç ai , GP 6: treated with AlCl3 and vitamin C, GP 7: treated with AlCl3, Aç ai and vitamin C. After 4 weeks, blood and liver specimens were collected to evaluate biochemical alterations and hepatic antioxidant and inflammatory parameters. AlCl3 treatment decreased liver enzymes (alanine aminotransferase, aspartate amino transferase, alkaline phosphatase), tumor necrosis factor-α and IL-6 while hepatic malondialdehyde was elevated. In contrast, hepatic glutathione, super oxide dismutase, catalase were decreased. Aç ai and vitamin C treatment improved the adverse effects induced by AlCl3, while co-administration with vitamin C promoted the action of aç ai on hepatic damage and antioxidant parameters. Aç ai showed a protective effect against AlCl3 induced toxicity, particularly in combination with vitamin C.

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The açaí flavonoid velutin is a potent anti-inflammatory agent: blockade of LPS-mediated TNF-α and IL-6 production through inhibiting NF-κB activation and MAPK pathway

Cited by 175 publications

References 37 publications

CD14 knockdown reduces lipopolysaccharide-induced cell viability and expression of inflammation-associated genes in gastric cancer cells in vitro and in nude mouse xenografts

CD14 knockdown reduces lipopolysaccharide-induced cell viability and expression of inflammation-associated genes in gastric cancer cells in vitro and in nude mouse xenografts

Anti-inflammatory activity of Cymbopogon citratus leaves infusion via proteasome and nuclear factor-κB pathway inhibition: Contribution of chlorogenic acid

Protective Effects of Açai in Combination with Vitamin C against Aluminum-Induced Toxicity in Rat Liver

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