Contribution of Conjugated Linoleic Acid to the Suppression of Inflammatory Responses through the Regulation of the NF-κB Pathway

Cheng, Wen-Ling; Lii, Chong‐Kuei; Chen, Haw‐Wen; Lin, Ting‐Hui; Liu, Kaili

doi:10.1021/jf0348626

Cited by 114 publications

(81 citation statements)

References 44 publications

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“…Our results are in accord with Poerschmann et al, who showed that the unsaturation index of FAs in algae and bacteria tends to be higher in colder climates than in warmer climates [70,74]. -3 PUFAs, but not -6 PUFAs, mono-unsaturated FAs or saturated FAs, have been shown to be potent NF-B inhibitors [75][76][77][78][79][80]. One would hence have expected the CCMP 1619 extract, which has a twelve times higher concentration in -3 PUFA than the remaining extracts, to stand out as the strongest NF-B inhibitor.…”

Section: Discussionsupporting

confidence: 93%

The inhibition of TNF-α-induced NF-κB activation by marine natural products

Folmer

Jaspars

Solano

et al. 2009

Biochemical Pharmacology

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, et al.. The inhibition of TNF-α induced NF-κB activation by marine natural products. Biochemical Pharmacology, Elsevier, 2009, 78 (6) 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 proof before it is published in its final 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. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 AbstractThe deregulated activation of NF-B is associated with cancer development and inflammatory diseases. With the aim to find new NF-B inhibitors, we purified and characterized compounds from extracts of the Fijian sponge Rhabdastrella globostellata, the crinoid Comanthus parvicirrus, the soft corals Sarcophyton sp. nov. and Sinularia sp., and the gorgonian Subergorgia sp. after an initial screening of 266 extracts from different marine origins.Results obtained show that selected purified compounds had a cytotoxic effect on the human leukaemia cell line K562, inhibited both TNF--induced NF-B-DNA binding as well as TNF- induced IB degradation and nuclear translocation of p50/p65. Furthermore, we observed inhibition of NF-B activation induced by an overexpression of TNFR1, TRAF2, TRADD, or IKK Interestingly, natural products inhibited IKK kinase as well as the 26S proteasome proteolytic activity.

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Section: Discussionsupporting

confidence: 93%

The inhibition of TNF-α-induced NF-κB activation by marine natural products

Folmer

Jaspars

Solano

et al. 2009

Biochemical Pharmacology

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“…In addition, CLA-induced antioxidative changes observed with the treatment seem to be modulated in a PPARc independent and NF-jBp50/ p65 dependent manner. In fact, CLA has been reported to down-regulate NF-jB p50/p65 activation and the expression of its target gene COX-2 as a ROS generator (Iwakiri et al, 2002;Cheng et al, 2004;Ringseis et al, 2006;Park et al, 2010). Although other investigators have reported that the trans-10, cis-12 CLA isomer induces prooxidative and inflammatory effects through NF-jB p50/p65 activation (Kennedy et al, 2009;Martinez et al, 2010), this does not appear to be a factor at the 50 lmol/L dose used under the conditions of the current study.…”

Section: Discussioncontrasting

confidence: 66%

Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury

Omaye¹

2012

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 5f. WORK UNIT NUMBER REPORT DATE July 2012 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERNevada System of Higher Education Reno, NV 89557-001 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTExperiments were performed to study Gamma-glutamycysteine (GGC) a precursor dipeptide for glutathione (GSH) for its ability to inhibit oxidative stress in human umbilical vein endothelial cells (HUVEC). HUVEC were used as a model to assess cellular biochemical changes that occur in hemorrhagic shock. We found that GGC protects against oxidative stress by alteration of gene expression of antioxidant defense independent of increased induction of endogenous GSH synthesis. In mixture studies looking at the effects of GGC with conjugated linoleic acid in HUVEC, we found that the mixture protected against oxidative stress similar to treatment with GGC alone. Therefore, GGC is likely a unique compound that exerts protection from oxidative stress by novel by modulation of gene expression of antioxidant defense enzymes. We have also develop a sensitive high performance liquid chromatographic method (HPLC) using fluorimetric detection to measure cellular changes in GGC. SUBJECT TERMSOxidative stress, antioxidants, glutathione, gamma-glutamycysteine. Hemorrhagic shock is a leading cause of death in military combat and civilian trauma (Bellamy, 1984; Lieu, et al., 2004). Better understanding of the associated cellular biochemical changes that occur in ischemiareperfusion (IR) injury can lead to efficacious therapies (Thomas et al., 2008). Therefore, we studied the feasibility of using gamma-glutamylcysteine (GGC) a dipeptide precursor for glutathione as a potential compound in modulating the oxidative stress associated with IR injury. BODY:Specific goal -Determine GGC doses to inhibit cellular oxidative stress and in...

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“…Because inflammatory responses are associated with the pathophysiology of many diseases, Cheng et al (2004) found that conjugated linoleic acid may inhibit LPS-induced inflammatory events in RAW 264.7 macrophages and this inhibitory activity of conjugated linoleic acid, at least in part, occurs through conjugated linoleic acid modulating the NFkB activation, negatively regulating the expression of inflammatory mediators. The mRNA concentration of genes involved in lipid metabolism and the number of large adipocytes was reduced with LPS pretreatment (Luche et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Attenuated mRNA expression of lipid metabolism genes in primary hepatocytes following lipopolysaccharide treatment in dairy cows

Wang¹,

Li²,

Wang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The influence of ruminal acidosis on ruminal microbiology and metabolite production has received considerable attention, but little is known regarding the systemic manifestations that arise from ruminal acidosis. Lipopolysaccharide (LPS) is released in the gastrointestinal tract upon ingestion of high-grain or high-fat diets, and it has been implicated in the etiology of multiple energy-and lipid-related metabolic disturbances in ruminants. The liver plays a crucial role in the acute phase response to intruding pathogens. The effect of blood LPS in subacute ruminal acidosis on lipid metabolism in the liver has not been established. In this study, cell cultures were photographed using an inverted microscope. We observed that hepatocytes changed their morphologies from irregular triangle to circular (contraction) shapes; the number of contracted cells increased with the increasing LPS doses. This suggests that LPS can 3719 Lipid metabolism genes in primary hepatocytes ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 3718-3728 (2015) promote cell contraction and take off the wall, ultimately leading to cell apoptosis. With changes in LPS exposure, hepatocyte number also changes. We explored lipid metabolism in the liver using quantitative reverse transcription-polymerase chain reaction to detect the expression of key lipid metabolism enzymes in hepatocytes. We found that Toll-like receptor 4 signaling pathway mediated by LPS could attenuate mRNA expression of fatty acid synthesis genes and increase the expression of fatty acid transport genes in primary hepatocytes following LPS treatment in dairy cows.

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Contribution of Conjugated Linoleic Acid to the Suppression of Inflammatory Responses through the Regulation of the NF-κB Pathway

Cited by 114 publications

References 44 publications

The inhibition of TNF-α-induced NF-κB activation by marine natural products

The inhibition of TNF-α-induced NF-κB activation by marine natural products

Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury

Attenuated mRNA expression of lipid metabolism genes in primary hepatocytes following lipopolysaccharide treatment in dairy cows

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