DHA and EPA Down-regulate COX-2 Expression through Suppression of NF-κB Activity in LPS-treated Human Umbilical Vein Endothelial Cells

Lee, Soon Ae; Kim, Hye Jung; Chang, Ki Churl; Baek, Jong Chul; Park, Ji Kwon; Shin, Jeong Kyu; Choi, Woo June; Lee, Jong Hak; Paik, Woon Ki

doi:10.4196/kjpp.2009.13.4.301

Cited by 45 publications

(34 citation statements)

References 26 publications

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“…It is indicated that PGE2 reduction and COX-2 inhibition are indicative of the anti-inflammatory and neuroprotective action by DHA. Our findings support the previous studies that show DHA inhibited COX-2 expression and activity (Boudrault et al 2010;Singh et al 1997;Bazan 2009;Lee et al 2009b). Cyclooxygenase-2 protein expression is regulated by NFjB.…”

Section: Discussionsupporting

confidence: 96%

“…The mechanism of action of DHA on NF-jB was affected by its concentration. Lower concentration of DHA may cause activation of NF-jB transcription factor (Lee et al 2009b). Docosahexanoic acid was significantly inhibited NF-jB activity in a dosedependent manner (Lee et al 2009b).…”

Section: Discussionmentioning

confidence: 99%

“…It was demonstrated that DHA is effective in inhibiting COX-1 and COX-2 catalyzed PG synthesis and was activated in response to PLA 2 activation. Cyclooxygenase-2 activation is also associated with ischemia, oxidative stress, inflammation, neuroactive cell signaling molecules, and developmental processes associated with aging (Mattammal et al 1995;McLaughlin et al 2006;Lee et al 2009b).…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Docosahexaenoic Acid on Visual Evoked Potentials in a Mouse Model of Parkinson’s Disease: The Role of Cyclooxygenase-2 and Nuclear Factor Kappa-B

et al. 2011

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This study aimed to investigate the effect of docosahexaenoic acid (DHA) on visual evoked potentials (VEPs) in a mice model of Parkinson's disease (PD). Mice model was created by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and DHA was given by gavage. Cyclooxygenase-2 (COX-2), caspase-3 activities, nuclear factor kappa-B (NF-κB) and prostaglandin E2 (PGE2) levels were determined in substantia nigra (SN) and retina. Cyclooxygenase-2 intensities were also determined immunohistochemically. The tyrosine hydroxylase (TH) immunolabelling was significantly decreased in MPTP group compared to control. Docosahexaenoic acid decreased dopaminergic neuron death in MPTP + DHA group when compared to MPTP group. Mice treated with MPTP showed motor deficits as compared to control. Significant improvement was observed in MPTP + DHA group when compared to MPTP group. Treatment with MPTP significantly increased the activity of COX-2 and total COX in SN when compared to the control group. Docosahexaenoic acid caused a significant decrease in total COX and COX-2 activity in SN of mice given MPTP. Cyclooxygenase-2 showed strong immunostaining in MPTP group when compared to other groups in SN. Levels of PGE2 increased in MPTP group when compared to control in SN. Docosahexaenoic acid treatment in MPTP group reduced PGE2 in SN. Nuclear factor kappa-B levels were found to be decreased in SN of MPTP group. The mean latencies of P1, N1, P2, N2, P3, N3, P4, N4, and P5 VEP components were significantly prolonged in MPTP group when compared to control. In MPTP + DHA group, the mean latencies of all components except P5 returned to control values. Current data shows that DHA treatment improves prolonged VEPs latencies and locomotor activity.

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Section: Discussionsupporting

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Effect of Docosahexaenoic Acid on Visual Evoked Potentials in a Mouse Model of Parkinson’s Disease: The Role of Cyclooxygenase-2 and Nuclear Factor Kappa-B

et al. 2011

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“…1E). Because DHA was shown to be a ligand for PPAR-γ [25] which may regulate CD73 transcription processes, the PPAR-γ antagonist GW9662 was applied. In line with the negative RT-PCR result, GW9662 had no effect on CD73 protein level (Fig.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Ecto-5´-Nucleotidase by Docosahexaenoic Acid in Human Endothelial Cells

Thom¹,

Wendel²,

Deußen³

2013

Cell Physiol Biochem

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Background/Aims: Modulation of extracellular adenine nucleotide and adenosine concentrations is one potential mechanism by which docosahexaenoic acid (DHA) may exert beneficial effects in critically ill patients. This study assessed DHA effects on extracellular adenine purines. Methods: Experiments used human pulmonary endothelial cells (HPMEC) and umbilical vein endothelial cells (HUVEC) treated with DHA (48 h). mRNA level (real-time PCR), expression (western blot, flow cytometry) and activities (hydrolysis of etheno(ε)-purines and fluorescence HPLC) of CD73 (ecto-5´-nucleotidase) and CD39 (ecto-NTPDase-1) were quantified. Results: DHA elevated total CD73 membrane protein expression concentration-dependently but CD73 mRNA level did not change. Increased expression was paralleled by increased enzyme activity. Effects observed on membrane level were reversed in intact cells, in which ε-AMP hydrolysis decreased after DHA. In intact endothelial cells ATP release was enhanced and CD39 activity blunted following DHA treatment. Hence, extracellular ATP and ADP concentrations increased and this inhibited ε-AMP hydrolysis. Conclusion: In human endothelial cells DHA caused 1) up-regulation of CD73 protein content and increased AMP hydrolysis at the cell membrane level, 2) increased cellular ATP release, and 3) decreased extracellular ATP/ADP hydrolysis. Thus, reorganization of the extracellular adenine-nucleotide-adenosine axis in response to DHA resulted in an increased extracellular ATP/adenosine ratio.

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“…Therefore, it was thought that the beneficial effects of taking fish oil are the result of displacing ARA by EPA and/or DHA, which then lowers the generation of proinflammatory eicosanoids. In addition, EPA and DHA were also shown to inhibit ARA metabolism, including decreasing the gene expression of COX-2 [1,3] , which generates the proinflammatory eicosanoids. Human studies have shown that oral intake of fish oil (EPA + DHA) decreases the production of ARA-derived eicosanoids [1,4] .…”

Section: Introductionmentioning

confidence: 99%

The Role of Fish Oil in Inflammatory Eye Diseases

Wang

Daggy

2017

Biomed Hub

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Consumption of fish oil is associated with reduced morbidity and mortality of cardiovascular diseases and also reduces the severity of many other inflammatory diseases and autoimmune disorders. The beneficial effects are attributed to the anti-inflammatory effects of the omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), found in fish oils. The mechanism of the anti-inflammatory effects was long thought to be by modulating the production of proinflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. Recent advances in research into the novel lipid mediators (resolvins, protectins, and maresins) derived from EPA and DHA and their role in the resolution of inflammation have shed new light on the pleiotropic nature of these fatty acids. In this review, we focus on the effects of EPA and DHA from fish oil in the treatment of two common inflammatory eye diseases - dry eye disease and age-related macular degeneration. Evidence from recent studies lends support to a role of fish oil in the treatment of these two eye diseases.

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DHA and EPA Down-regulate COX-2 Expression through Suppression of NF-κB Activity in LPS-treated Human Umbilical Vein Endothelial Cells

Cited by 45 publications

References 26 publications

The Effect of Docosahexaenoic Acid on Visual Evoked Potentials in a Mouse Model of Parkinson’s Disease: The Role of Cyclooxygenase-2 and Nuclear Factor Kappa-B

The Effect of Docosahexaenoic Acid on Visual Evoked Potentials in a Mouse Model of Parkinson’s Disease: The Role of Cyclooxygenase-2 and Nuclear Factor Kappa-B

Regulation of Ecto-5´-Nucleotidase by Docosahexaenoic Acid in Human Endothelial Cells

The Role of Fish Oil in Inflammatory Eye Diseases

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