Docosahexaenoic acid attenuates VCAM-1 expression and NF-κB activation in TNF-α-treated human aortic endothelial cells

Wang, Tzu-Ming; Chen, Chun‐Jung; Lee, Tzong‐Shyuan; Chao, H.-C.; Wu, Wen-Huey; Hsieh, Shu-Chen; Sheu, Huey-Herng; Chiang, An-Na

doi:10.1016/j.jnutbio.2010.01.007

Cited by 73 publications

(55 citation statements)

References 61 publications

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“…Activated NFB can lead to the enhanced efflux of MCP-1 and VEGF in serum (Wang et al, 2008). Early events in AS are usually driven by NFB, and the disruption of NFB signaling pathway has been shown to delay vascular impairment (Zheng et al, 2009;Wang et al, 2010). MCP-1, a member of chemoattractant family and can recruit and activate the monocyte, has been demonstrated to be enhanced in aortic pathology rabbits induced by hypercholesterolemia (Oh et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Chen

Lei

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Chen

Lei

et al. 2011

Journal of Ethnopharmacology

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“…[13][14][15] Indeed docosahexaenoic acid, the precursor for RvD1 and RvD2 16,17 as well as MaR1 8 reduces atherosclerosis in mice, 18 and plasma docosahexaenoic acid levels associate with reduced atheroprogression in coronary arteries in humans. 19 Similarly, 12/15 lipoxygenase, the enzyme responsible for the synthesis of Lipoxin A4, RvD1, and MaR1 was also shown to be protective toward atherosclerosis, 20 setting the stage for the indication that progression of atherosclerosis may be a consequence of failed resolution.…”

mentioning

confidence: 99%

Resolving Lipid Mediators Maresin 1 and Resolvin D2 Prevent Atheroprogression in Mice

Viola¹,

Lemnitzer²,

Jansen³

et al. 2016

Circulation Research

190

163

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Rationale: Atheroprogression is a consequence of nonresolved inflammation, and currently a comprehensive overview of the mechanisms preventing resolution is missing. However, in acute inflammation, resolution is known to be orchestrated by a switch from inflammatory to resolving lipid mediators. Therefore, we hypothesized that lesional lipid mediator imbalance favors atheroprogression. Objective: To understand the lipid mediator balance during atheroprogression and to establish an interventional strategy based on the delivery of resolving lipid mediators. Methods and Results: Aortic lipid mediator profiling of aortas from Apoe −/− mice fed a high-fat diet for 4 weeks, 8 weeks, or 4 months revealed an expansion of inflammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant decrease of resolving lipid mediators, Resolvin D2 (RvD2) and Maresin 1 (MaR1), during advanced atherosclerosis. Functionally, aortic Leukotriene B4 and Prostaglandin E2 levels correlated with traits of plaque instability, whereas RvD2 and MaR1 levels correlated with the signs of plaque stability. In a therapeutic context, repetitive RvD2 and MaR1 delivery prevented atheroprogression as characterized by halted expansion of the necrotic core and accumulation of macrophages along with increased fibrous cap thickness and smooth muscle cell numbers. Mechanistically, RvD2 and MaR1 induced a shift in macrophage profile toward a reparative phenotype, which secondarily stimulated collagen synthesis in smooth muscle cells. Conclusions: We present evidence for the imbalance between inflammatory and resolving lipid mediators during atheroprogression. Delivery of RvD2 and MaR1 successfully prevented atheroprogression, suggesting that resolving lipid mediators potentially represent an innovative strategy to resolve arterial inflammation.

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“…We also showed that the serum EPA/AA ratio in obese patients is associated with monocyte expression of IL-10, an antiinflammatory M2 marker 16) . DHA and EPA are n-3 PUFAs, and may contribute to the prevention of atherosclerosis and inflammatory diseases 11,17) . The Framingham Heart Study reported that a high plasma phosphatidylcholine DHA level was associated with a significant reduction in the risk of developing all-cause dementia 18) .…”

Section: Study Protocolmentioning

confidence: 99%

An Increase in the EPA/AA Ratio is Associated with Improved Arterial Stiffness in Obese Patients with Dyslipidemia

Itô

Satoh‐Asahara

Yamakage

et al. 2014

JAT

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Aim: Previous epidemiological studies demonstrated that the ratio of n-6 to n-3 polyunsaturated fatty acids is associated with cardiovascular diseases. We herein investigated whether the beneficial effect of highly purified eicosapentaenoic acid (EPA) on arterial stiffness is associated with changes in the ratio of polyunsaturated fatty acids, such as EPA, docosahexaenoic acid (DHA) and dihomo-γ-linolenic acid (DGLA), relative to arachidonic acid (AA), in obese Japanese patients with dyslipidemia. Methods: The EPA/AA, DHA/AA and DGLA/AA ratios were compared between obese patients with (n=94) and without (n= 31) dyslipidemia. Among the former group, 88 patients received either highly purified EPA treatment (1.8 g daily, n = 45) or treatment without EPA (control, n = 43). Results: At baseline, the ratios of DHA/AA and DGLA/AA were significantly (P＜0.05) higher in obese patients with dyslipidemia than in those without, while the EPA/AA ratio was similar between patients with and without dyslipidemia. EPA significantly reduced the hemoglobin A1c, total cholesterol, triglycerides, CRP, cardio-ankle vascular index (CAVI) (an index of arterial stiffness) and the DGLA/AA ratio relative to the control at three months after the treatment. On the other hand, EPA significantly increased the adiponectin level and EPA/AA ratio (P＜0.05). A multivariate regression analysis revealed that only age, an increase in the EPA/AA ratio and a decrease in the CRP level were significant determinants of a reduction of the CAVI by EPA. Conclusion: These findings suggest that EPA improves the arterial stiffness in association with an increase in the EPA/AA ratio and a decrease in inflammation in obese patients with dyslipidemia. J Atheroscler Thromb, 2014; 21:248-260.

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Docosahexaenoic acid attenuates VCAM-1 expression and NF-κB activation in TNF-α-treated human aortic endothelial cells

Cited by 73 publications

References 61 publications

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Resolving Lipid Mediators Maresin 1 and Resolvin D2 Prevent Atheroprogression in Mice

An Increase in the EPA/AA Ratio is Associated with Improved Arterial Stiffness in Obese Patients with Dyslipidemia

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