Effects Of Eicosapentaenoic Acid Research Articles

Effects of the Addition of Eicosapentaenoic Acid to Strong Statin Therapy on Inflammatory Cytokines and Coronary Plaque Components Assessed by Integrated Backscatter Intravascular Ultrasound.

The effects of eicosapentaenoic acid (EPA) on coronary artery disease have been previously reported; however, those of the addition of EPA to strong statins on coronary plaque components and local inflammatory cytokines are not known. A total of 95 patients who had been treated with strong statin for at least 6 months were randomized into 2 groups: an EPA group (additional treatment with EPA at 1,800 mg/day, n=48) or a control group (no additional treatment, n=47), for 6 months. The tissue characteristics of target coronary plaque in each patient were analyzed using IB-IVUS before and after treatment. We also measured plasma levels of inflammatory cytokines sampled in the coronary sinus (CS) and peripheral vein.A significant reduction in lipid volume (18.5 ± 1.3 to 15.0 ± 1.5 mm(3), P=0.007) and a significant increase in fibrous volume (22.9 ± 0.8 to 25.6 ± 1.1 mm(3), P=0.01) were observed in IB-IVUS image analyses in the EPA group, but no significant changes in the plaque components in the control group. CS levels of pentraxin 3 and monocyte chemoattractant protein-1 were lower after than before treatment with EPA (3.3 ± 2.1 to 2.6 ± 1.2 ng/ml, 120.4 ± 26.2 to 110.2 ± 26.8 pg/ml, P=0.015 and P=0.008, respectively); however, there were no significant changes in those inflammatory cytokines between pre- and post-treatment in the control group. The addition of EPA was associated with reduced lipid volume in coronary plaques and decreased inflammatory cytokines.

Dietary Effects of Oxidized Eicosapentaenoic Acid (EPA) and Intact EPA on Hepatic Steatosis Induced by a High-sucrose Diet and Liver-X-receptor α Agonist in Mice.

Numerous studies have shown that dietary omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA), improve lipid metabolism. The beneficial effects of PUFA-derived oxidation products have been increasingly reported. However, EPA is easily oxidized in food products and in the human body, generating various derivatives of oxidized EPA (oxEPA), such that these oxidation products may partially contribute to EPA's effect. We previously reported that oxEPA was more potent than intact EPA in reducing liver-X-receptor α (LXRα)-induced cellular triacylglycerol (TG) accumulation. However, the in vivo hypolipidemic effects of oxEPA remain unclear. In the present study, we evaluated the effect of oral administration of EPA and oxEPA on hepatic steatosis in mice induced by a high-sucrose diet and a synthetic LXRα agonist, TO-901317. Both EPA and oxEPA reduced TG accumulation in the liver and plasma biomarkers of liver injury. Furthermore, they suppressed the expression of lipogenic genes, but not β-oxidation genes, in a similar pattern as the biomarkers. Our results suggest that oxEPA and intact EPA suppress de novo lipogenesis to ameliorate hepatic steatosis.

The study of the apoptosis induced by EPA on human colon cancer SW480 cells

Objective To investigate the effect of eicosapentaenoic acid(EPA) on the apoptosis of human colon cancer SW480 cells and the mechanisms. Methods Mitochondrial membrane potential was detected, the quantity of cytochrome C was analyzed by Elisa kit, and the expression of cleaved caspase-9 and caspase-3 was detected by Western Blot. Results After treatment with EPA(0μg/mL, 42.1μg/mL, 84.2μg/mL, 168.4μg/mL), the mitochondrial membrane potential(Δψm) of SW480 cells were declined(P<0.05), the values were (99.71±0.04)%, (95.04±0.10)%, (88.65±0.41)% and (73.60±1.20)%(t=5.161, 6.302, 4.601, 5.198, all P<0.05). The quantity of cytochrome C in cytosol was increased significantly compared with no treatment group, and the values were (12.8±1.2)ng/mL, (115.5±3.5)ng/mL, (290.5±5.2)ng/mL and (262.0±12.5)ng/mL in different EPA treatment groups(t=6.345, 6.013, 5.846, 4.613, all P<0.01). The expression of cleaved caspase-9 and caspase-3 were significantly increased. Conclusion EPA inhibits SW480 cells growth and induces apoptosis in a dose dependent manner.This action may be mediated by mitochondria-mediated intrinsic apoptosis pathway, cytochrome C release, and caspase-9 and caspase-3 activation. Key words: Colon tumor; Twenty carbon five acid; SW480 cells; Cell apoptosis

Researches on the Pharmacological Effects of Eicosapentaenoic Acid

Researches on the Pharmacological Effects of Eicosapentaenoic Acid

Biologic plausibility, cellular effects, and molecular mechanisms of eicosapentaenoic acid (EPA) in atherosclerosis.

Residual cardiovascular (CV) risk remains in dyslipidemic patients despite intensive statin therapy, underscoring the need for additional intervention. Eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, is incorporated into membrane phospholipids and atherosclerotic plaques and exerts beneficial effects on the pathophysiologic cascade from onset of plaque formation through rupture. Specific salutary actions have been reported relating to endothelial function, oxidative stress, foam cell formation, inflammation, plaque formation/progression, platelet aggregation, thrombus formation, and plaque rupture. EPA also improves atherogenic dyslipidemia characterized by reduction of triglycerides without raising low-density lipoprotein cholesterol. Other beneficial effects of EPA include vasodilation, resulting in blood pressure reductions, as well as improved membrane fluidity. EPA's effects are at least additive to those of statins when given as adjunctive therapy. In this review, we present data supporting the biologic plausibility of EPA as an anti-atherosclerotic agent with potential clinical benefit for prevention of CV events, as well as its cellular effects and molecular mechanisms of action. REDUCE-IT is an ongoing, randomized, controlled study evaluating whether the high-purity ethyl ester of EPA (icosapent ethyl) at 4 g/day combined with statin therapy is superior to statin therapy alone for reducing CV events in high-risk patients with mixed dyslipidemia. The results from this study are expected to clarify the role of EPA as adjunctive therapy to a statin for reduction of residual CV risk.

Effects of Eicosapentaenoic Acid on the Cytoprotection Through Nrf2-Mediated Heme Oxygenase-1 in Human Endothelial Cells.

Consumption of omega-3 polyunsaturated fatty acid, particularly eicosapentaenoic acid (EPA), is associated with a significant reduction in the risk of developing cardiovascular disease. The aim of this study was to investigate whether heme oxygenase-1 (HO-1) induction contributes to the cytoprotective effects of EPA in endothelial cells threatened with oxidative damage. In this study, we investigated the effect of EPA on the induction of HO-1 by NF-E2-related factor 2 (Nrf2) in human umbilical vein endothelial cells. In cells treated with low concentrations of EPA (10-25 μM), HO-1 expression increased in a time- and concentration-dependent manner. Additionally, EPA treatment increased Nrf2 nuclear translocation and antioxidant response element activity, leading to the upregulation of HO-1 expression. Furthermore, treatment with EPA reduced hydrogen peroxide (H(2)O(2))-induced cell death. The reduction in cell death was reversed by treatment with zinc protoporphyrin, an inhibitor of HO-1, indicating that HO-1 contributed to the protective effect of EPA. These data suggest that EPA protects against H(2)O(2)-induced oxidative stress in endothelial cells by activating Nrf2 and inducting HO-1 expression.

Effects of eicosapentaenoic acid on hepatic dyslipidemia and oxidative stress in high fat diet-induced steatosis

We investigated the ability of eicosapentaenoic acid (EPA) to prevent high-fat diet (HFD)-induced obesity and non-alcoholic fatty liver disease (NAFLD). Male C57BL/6J mice were fed standard chow (5.3% fat content), an HFD (32.0% fat content) or an HFD + EPA (1 g/kg/day EPA for the last 6 weeks) for 12 weeks. Serum total cholesterol, hepatic triglyceride and total cholesterol levels were significantly increased in the HFD group, in comparison with those of normal mice (p < 0.01). In contrast, hepatic triglyceride and total cholesterol levels were significantly decreased in the HFD + EPA group, in comparison with those of the HFD group (p < 0.05). In addition, EPA decreased the body weight of obese mice and improved hepatic function. Hepatic superoxide dismutase activity and glutathione levels were significantly decreased in obese mice, but increased with EPA administration. Our data suggest that EPA supplementation has a beneficial effect on NAFLD progression.

ω-3 PUFAs and Resveratrol Differently Modulate Acute and Chronic Inflammatory Processes.

ω-3 PUFAs and polyphenols have multiple effects on inflammation in vivo and in vitro. The effects of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and resveratrol (RV) were investigated in LPS-stimulated peripheral blood leukocytes (PBLs) (i.e., acute inflammation) and IL-1β activated human chondrocytes (i.e., chronic inflammation). Inflammatory mediators including chemokines, cytokines, interleukins, and PGE2 were measured by multiplex analysis and gene expression was quantified by RT-PCR. In PBLs, RV decreased the secretion of PGE2, CCL5/RANTES, and CXCL8/IL-8 but increased IL-1β, IL-6, and IL-10. In contrast to RV, ω-3 PUFAs augmented the production of PGE2 and CXCL8/IL-8. EPA and DHA similarly affected the pattern of inflammatory mediators. Combination of RV and ω-3 PUFAs exerted synergistic effects on CCL5/RANTES and had additive effects on IL-6 or CXCL8/IL-8. Both ω-3 PUFAs and RV reduced catabolic gene expression (e.g., MMPs, ADAMTS-4, IL-1β, and IL-6) in activated chondrocytes. The data suggest that ω-3 PUFAs and RV differ in the regulation of acute inflammation of peripheral blood leukocytes but have common properties in modulating features related to chronic inflammation of chondrocytes.

Long-Chain Omega-3 Fatty Acids and Optimization of Cognitive Performance

Low consumption of the omega-3 fatty acids, eicosapentaenoic and docosahexaenonic acids, is linked to delayed brain development and, in late life, increased risk for Alzheimer's disease. The current review focuses on cognitive functioning during midlife and summarizes available scientific evidence relevant to the hypothesis that adequate dietary consumption of the long-chain omega-3 fatty acids is necessary for optimal cognitive performance. Taken together, the findings suggest that raising the currently low consumption among healthy adults may improve some aspects of cognitive performance. Nonetheless, evidence from randomized clinical trials is comparatively sparse and leaves unclear: (a) whether such effects are clinically significant, (b) whether effects of eicosapentaenoic acid and DHA differ, (c) which dimensions of cognitive function are affected, (d) the dose-response relationships, or (e) the time course of the response. Clarification of these issues through both laboratory and clinical investigations is a priority given the broad implications for public health, as well as for military personnel and other positions of high performance demand and responsibility.

Effect of eicosapentaenoic acid on cholesterol gallstone formation in C57BL/6J mice.

The present study investigated the preventive effect of ω-3 fatty acids against cholesterol gallstone (CG) formation. CG formation was induced in C57BL/6J mice using a lithogenic diet (LD). The mice were divided into four treatment groups: i) LD, ii) LD plus eicosapentaenoic acid (EPA), iii) LD plus docosahexaenoic acid (DHA) and iv) LD plus EPA plus DHA. Subsequent to feeding the mice the LD for four weeks, EPA and/or DHA (70 mg/kg/day) were orally administered for eight weeks. The mice in the EPA treatment groups exhibited significantly less gallstone formation than those in the LD group. By contrast, DHA treatment only slightly suppressed gallstone formation. The expression of mucin 2, 5AC, 5B and 6 was significantly decreased in the gallbladders of mice in the EPA groups (70-90%) and the LD plus DHA group (30-50%), compared with that in the mice in the LD group. In addition, the mRNA expression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase was significantly decreased in the livers of mice in the EPA treatment group compared with that in the livers of mice in the LD group. In conclusion, EPA was found to have a dominant anti-lithogenic effect in C57BL/6J mice.

Effects of eicosapentaenoic acid and docosahexaenoic acid on prostate cancer cell migration and invasion induced by tumor-associated macrophages.

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are the major n-3 polyunsaturated fatty acids (PUFAs) in fish oil that decrease the risk of prostate cancer. Tumor-associated macrophages (TAMs) are the main leukocytes of intratumoral infiltration, and increased TAMs correlates with poor prostate cancer prognosis. However, the mechanism of n-3 PUFAs on prostate cancer cell progression induced by TAMs is not well understood. In this study, we investigated the effects of EPA and DHA on modulating of migration and invasion of prostate cancer cells induced by TAMs-like M2-type macrophages. PC-3 prostate cancer cells were pretreated with EPA, DHA, or the peroxisome proliferator-activated receptor (PPAR)-γ antagonist, GW9662, before exposure to conditioned medium (CM). CM was derived from M2-polarized THP-1 macrophages. The migratory and invasive abilities of PC-3 cells were evaluated using a coculture system of M2-type macrophages and PC-3 cells. EPA/DHA administration decreased migration and invasion of PC-3 cells. The PPAR-γ DNA-binding activity and cytosolic inhibitory factor κBα (IκBα) protein expression increased while the nuclear factor (NF)-κB p65 transcriptional activity and nuclear NF-κB p65 protein level decreased in PC-3 cells incubated with CM in the presence of EPA/DHA. Further, EPA/DHA downregulated mRNA expressions of matrix metalloproteinase-9, cyclooxygenase-2, vascular endothelial growth factor, and macrophage colony-stimulating factor. Pretreatment with GW9662 abolished the favorable effects of EPA/DHA on PC-3 cells. These results indicate that EPA/DHA administration reduced migration, invasion and macrophage chemotaxis of PC-3 cells induced by TAM-like M2-type macrophages, which may partly be explained by activation of PPAR-γ and decreased NF-κB p65 transcriptional activity.

All omega 3 fatty acids improve serum lipid profiles and decrease aortic plaque buildup in LDLr‐/‐ mice fed an atherogenic diet (40.1)

Although the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on vascular disease markers have been well studied, the effect of docosapentaenoic acid omega‐3 (DPAn3) has been studied less. The objective of this study was to compare the effects of DPAn3, EPA, DHA, and commercial combinations of EPA, DPAn3, and DHA on serum lipid profiles and the development of atherosclerosis in mice. Male LDLr‐/‐ mice were assigned to one of six atherogenic (42% kcal from fat) dietary treatments (n=8) that had 3.5% of total fatty acids (FA) replaced with milk fat, DHA, DPAn3, EPA, or a commercial n3 fatty acid preparation. Blood samples were taken at 0, 10, and 20 weeks into the study; serum was isolated and probed for lipid classes and glucose. Aortic arches were harvested from all mice and total, free, and esterified cholesterol are reported. Serum lipid profiles and glucose in mice increased over the study, but supplementing n3 polyunsaturated fatty acids (PUFA) decreased (P&lt;0.05) serum cholesterol, triglyceride, and non‐esterified fatty acid concentrations compared to the milk fat control. Mice supplemented with all n3 PUFA had decreased aortic total cholesterol (P&lt;0.10) and cholesterol ester (P&lt;0.05) compared to the control mice. The results of this study suggest that EPA, DPA, and DHA may equally (P&gt;0.10) improve serum lipid profiles and decrease aortic plaque buildup in a mouse model prone to atherosclerosis.Grant Funding Source: Supported by Omega Protein Corporation

Effects of eicosapentaenoic acid and the GPR120 agonist TUG‐891 on lysophosphatidic acid signaling in human prostate cancer cells (1066.10)

There is a high incidence of prostate cancer in the Western world, which may be partially attributed to Western diets that are generally deficient in omega‐3 fatty acids (n‐3 FAs). Dietary n‐3 FAs have been shown to inhibit proliferation of prostate cancer cells in culture. The G protein‐coupled receptor GPR120, which is expressed in normal prostate and prostate tumors, serves as a receptor for the n‐3 FA eicosapentaenoic acid (EPA). We therefore hypothesized that the inhibitory effects of n‐3 FAs on prostate cancer cell proliferation are mediated by GPR120. To test this hypothesis, we performed proliferation and signal transduction studies, comparing the effects of lysophosphatidic acid (LPA), EPA, the GPR120 agonist TUG‐891, and the GPR40 agonist GW9508 in DU145 and PC‐3 cells. We found that EPA and TUG‐891 inhibit proliferation of human prostate cancer cells in response to LPA. In addition, brief (15 minute) pre‐incubation of serum‐starved cells with EPA or TUG‐891 suppresses subsequent activation of ERK, p70S6K, and FAK in response to LPA. This rapid effect of EPA is consistent with mediation by a GPCR. Our data suggest that GPR120 shows promise as a therapeutic target in prostate cancer.Grant Funding Source: Washington State University College of Pharmacy

Effects of Eicosapentaenoic Acid on the Levels of Inflammatory Markers, Cardiac Function and Long-Term Prognosis in Chronic Heart Failure Patients with Dyslipidemia

The effects of eicosapentaenoic acid (EPA) on the levels of inflammatory markers, cardiac function and long-term prognosis in chronic heart failure (CHF) patients with dyslipidemia remain unclear. A total of 139 CHF patients with a mean left ventricular ejection fraction (LVEF) of 37.6± 8.0% were divided into two groups based on whether EPA was included in their treatment regimen: the EPA group (n=71) and the no EPA group (n=68). Only patients with dyslipidemia at baseline (entry) were treated with EPA. The monocyte chemoattractant protein (MCP)-1 and asymmetric dimethylarginine (ADMA) levels were measured at baseline and after 12 months of treatment. At 12 months, in the EPA group, the LVEF had improved and the MCP-1 and ADMA levels had decreased (respectively, p＜0.001); however, in the no EPA group, the LVEF had worsened, while the MCP-1 and ADMA levels had increased (respectively, p＜0.001). Fifty-five patients experienced cardiac events, including 15 cardiac deaths and 40 readmissions for worsening of CHF during a median follow-up period of 28.0 months. The percent change in LVEF from baseline was found to be significantly associated with the percent change in ADMA (r=-0.462, p＜0.001). A multivariate Cox hazard analysis showed EPA treatment (hazard ratio: 0.21, 95% confidence interval: 0.05-0.93, p=0.031) to be an independent predictor of cardiac events. These data indicate that EPA treatment may improve the cardiac function and long-term prognosis of CHF patients with dyslipidemia, at least in part, due to reductions in inflammation and improvements in the endothelial function.

Effects of eicosapentaenoic acid on platelet function in patients taking long-term aspirin following coronary stent implantation.

Eicosapentaenoic acid (EPA) has been widely accepted to have antiatherosclerotic effects. The aim of this study was to investigate the antiplatelet effect of EPA combined with acetylsalicylic acid (ASA) following stent implantation. Eighteen patients who had undergone coronary stent implantation at least 8 months previously were included. All patients were given EPA ethyl ester (EPA-E) 1.8 g/day in addition to ASA 100 mg/day for 12 weeks. After the treatment, the plasma EPA/arachidonic acid (AA) ratio increased significantly from 0.40 ± 0.2 to 1.08 ± 0.39 (P < 0.001). There were no changes in the maximum platelet aggregation (MPA) induced by adenosine diphosphate (5 and 20 µmol/L), AA (0.3 and 0.5 mg/mL), or collagen (2 and 4 µg/mL). Furthermore, no significant differences were observed in the expression of PAC-1 and CD62P on the platelet surface membranes or in the soluble P-selectin concentration. With further analysis, a significant negative correlation was found between collagen (2 µg/mL)-induced MPA and plasma EPA/AA ratio (r = -0.507, P = 0.032). The patients were then divided into 2 groups according to the median EPA/AA ratio value of 0.92. In the high EPA/AA ratio group (n = 10), collagen-induced MPA was significantly suppressed after EPA-E administration (45.3 ± 15.9 versus 39.0 ± 16.3, P = 0.033). In contrast, there were no significant changes in platelet aggregation (56.0 ± 9.8 versus 57.1 ± 11.4, P = 0.745) in the low EPA/AA ratio group (n = 8). EPA treatment had a potential to suppress collagen-induced platelet aggregation in patients with a high plasma EPA/AA ratio.

Effects of eicosapentaenoic acid and docosahexaenoic acid on chylomicron and VLDL synthesis and secretion in Caco-2 cells.

The present research was undertaken to determine the effects of EPA (20 : 5 n-3) and DHA (22 : 6 n-3) on chylomicron and VLDL synthesis and secretion by Caco-2 cells. Cells were incubated for 12 to 36 h with 400 μM OA, EPA, and DHA; then 36 h was chosen for further study because EPA and DHA decreased de novo triglycerides synthesis in a longer incubation compared with OA (P < 0.01). Neither the uptake nor oxidation was different in response to the respective fatty acids (P > 0.05). Compared with OA, intercellular and secreted nascent apolipoprotein B48 and B100 were decreased by EPA and DHA (P < 0.01). Both DHA and EPA resulted in a lower secretion of chylomicron and VLDL (P < 0.01). In contrast to OA, EPA and DHA were preferentially incorporated into phospholipids instead of triacylglycerols (P < 0.01). These discoveries demonstrated that exposure of DHA and EPA reduced the secretion of chylomicron and VLDL partly by regulating the synthesis of TG and apoB.

Inhibitory effect of eicosapentaenoic acid on cardiomyocyte in endothelin induced hypertrophy via PPAR-α

Inhibitory effect of eicosapentaenoic acid on cardiomyocyte in endothelin induced hypertrophy via PPAR-α

Effects of eicosapentaenoic acid on epicardial adipose tissue volume

Effects of eicosapentaenoic acid on epicardial adipose tissue volume

Abstract 3668: Chemopreventive effect of omega-3 fatty acid, EPA, in non-small cell lung cancer through formation of PGE3 and inhibition of PI3kinase/mTOR pathways.

Abstract The beneficial effects of eicosapentaenoic acid (EPA) are due, in part, to selective alteration of arachidonic acid metabolism that involves cyclooxygenase enzymes. We previously reported that the anti-proliferative effect of EPA in human non-small cell lung cancer (NSCLC) A549 cells was associated with formation of PGE3, a COX-2 metabolite of the fish oil derived EPA (J. Lipid Res. 45: 1030-1039, 2004). Here we report that EPA differentially regulated the in vitro anti-proliferative effect in non-small cell lung cancer A549 and H596 cells and the in vivo chemopreventive effect in K-ras transgenic murine lung carcinoma. When both A549 and H596 cells were treated with EPA (1 to 100 μM) for 72 hrs, EPA inhibited proliferation of A549 cells (IC50 &amp;lt; 6.25 μM) more effectively than H596 cells (IC50 &amp;gt; 50 μM), although both expressed similar level of COX-2. Analysis by MALDI MS showed that the level of EPA incorporated into phospholipids in H596 cells was 4-fold higher than A549 cells. Unexpectedly, H596 cells produced much less PGE3 than A549 cells. This is likely due to the relatively lower expression and activity of cytosolic phospholipase A2 (cPLA2) in H596 cells than in A549 cells. Use of siRNA to knock down cPLA2 in A549 cells markedly reduced the anti-proliferative activity of EPA compare to the control siRNA transfected cells. Intriguingly, PGE3 exhibited a dose dependent inhibition of proliferation, invasion and migration in A549 cells, possibly through down regulation of phosphorylation of Akt and S6 proteins. To assess the chemopreventive effect of EPA in lung cancer development, FVB/Kras (LA2) mouse were fed either a soybean oil diet (control) or one containing 1% or 2% EPA for 20 weeks. There was a 54% reduction in the number of tumor nodules in the 2% EPA diet group compared to control (P &amp;lt; 0.05). In addition, average tumor volume was dramatically reduced by 67% in the 2% EPA diet fed animals compared with the control group (P &amp;lt; 0.05). These results were confirmed by micro-CT and histopathology examinations. Interestingly, the endogenous levels of PGE2 in mouse lung tumor tissues were significantly reduced from control level of 489.1 ± 125.5 ng/mg to 171.9 ± 57.3 ng/mg protein in EPA (2%) treated mice, whereas PGE3 levels were significantly increased to 76.2 ± 33.3 ng/mg protein in EPA (2%) diet group compared to control group (5.1 ± 2.0 ng/mg protein). Furthermore, EPA (2%) markedly inhibited expression of both pAkt and pS6 in lung tumor tissues compared to the control. Taken together, the data suggest that EPA has the ability to inhibit the proliferation of NSCLC cells and prevent the development of mouse lung carcinoma. The anti-proliferative effect of EPA might be mediated through increased production of PGE3, which is regulated by cPLA2 and COX-2 enzymes, and inhibition of mTOR and PI3kinase pathways. This study is supported by NCI Grant 1R01CA144053-01. Citation Format: Yong Pan, David Pirman, Ekem Efuet, Patrea Rhea, Carrie Cartwright, Murali Ravoori, Vikas Kundra, Susan Fischer, Peiying Yang. Chemopreventive effect of omega-3 fatty acid, EPA, in non-small cell lung cancer through formation of PGE3 and inhibition of PI3kinase/mTOR pathways. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3668. doi:10.1158/1538-7445.AM2013-3668

ω-3 Polyunsaturated Fatty Acids on the Prognosis of Multiple Sclerosis: The Effect of Eicosapentaenoic acid

The effect of nutrition and dietary supplements on the course of multiple sclerosis is a topic of great interest to both patients and clinicians. The influence of ω-3 polyunsaturated fatty acids (PUFAs) on the development and course of multiple sclerosis (MS) has been under investigation. A number of small, uncontrolled clinical trials with fish oil (rich in eicosapentaenoic acid (EPA; 20:5 ω-3) and docosahexaenoic acid (DHA; 22:6 ω-3) have indicated a possible beneficial effects of ω-3 PUFAs, but controlled trials have not been able to draw definitive conclusions. Among ω-3 PUFAs, EPA has the most potent effect on myelinogenesis and inflammatory process, thus the conflicting results could be due to the different mixtures of EPA and DHA contained in the various sources of fish oil. This review discusses on the possible role of EPA in demyelinating diseases.