Docosahexaenoic acid, an omega-3 polyunsaturated acid protects against indomethacin-induced gastric injury

Pineda-Peña, Elizabeth Arlen; Jiménez-Andrade, Juan Miguel; Castañeda‐Hernández, Gilberto; Chávez-Piña, Aracely Evangelina

doi:10.1016/j.ejphar.2012.09.049

Cited by 23 publications

(25 citation statements)

References 20 publications

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“…Indeed, omega-3 may increase bleeding (Clarke et al, 1990;Mozaffarian & Wu, 2011) but they have also gastro-protective effects in doses of 5-10 ml/kg in animal models with gastric ulcers induced by various agents, including dexamethasone (Bhattacharya et al, 2006;Faust et al, 1989;Manjari & Das, 2000;Pineda-Pena et al, 2012). The observations in the present case study seem at first conflicting to the above mentioned gastroprotective effects of omega-3 fatty acids.…”

Section: Reflectionscontrasting

confidence: 61%

Gastrointestinal Bleeding After High Intake of Omega-3 Fatty Acids, Cortisone and Antibiotic Therapy: A Case Study

Detopoulou¹,

Papamikos²

2014

International Journal of Sport Nutrition and Exercise Metabolism

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Omega-3 fatty acids exert a plethora of physiological actions including triglycerides lowering, reduction of inflammatory indices, immunomodulation, anti- thrombotic effects and possibly promotion of exercise performance. Their use is widespread and for commonly ingested doses their side- effects are minimal. We report a case of a 60 y amateur athlete who consumed about 20 g omega-3 fatty acids daily from supplements and natural sources for a year. After the intake of cortisone and antibiotics he presented duodenum ulcer and bleeding although he had no previous history of gastrointestinal problems. Although several animal data support gastro-protective effects of omega-3 fatty acids in the present case they were not able to prevent ulcer generation. The present observation may be explained by (i) the high dose of omega-3 fatty acids and their effect on bleeding, (ii) the fact that cortisone increases their oxidation and may render them proinflammatory, (iii) other antithrombotic microconstituents included in the consumed cod-oil and/or the diet of the subject and (iv) the differences in the coagulation and fibrinolytic systems of well- trained subjects. Further studies are needed to substantiate any possible interaction of cortisone and omega-3 fatty acids in wide ranges of intake.

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Section: Reflectionscontrasting

confidence: 61%

Gastrointestinal Bleeding After High Intake of Omega-3 Fatty Acids, Cortisone and Antibiotic Therapy: A Case Study

Detopoulou¹,

Papamikos²

2014

International Journal of Sport Nutrition and Exercise Metabolism

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“…Earlier studies reported beneficial effect of polyunsaturated fatty acids such as DHA, linoleic acid, and g-linolenic acid in ulcer relief, including NSAID-induced ulcers (alShabanah, 1997;Pineda-Peña et al, 2012). The beneficial effects of these fatty acids in ulcer models could be attributable in part to their epoxide metabolites, as suggested by this study.…”

Section: Discussionsupporting

confidence: 48%

Anti-Ulcer Efficacy of Soluble Epoxide Hydrolase Inhibitor TPPU on Diclofenac-Induced Intestinal Ulcers

Goswami

Wan

Yang

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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Proton pump inhibitors such as omeprazole (OME) reduce the severity of gastrointestinal (GI) ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs) but can also increase the chance of dysbiosis. The aim of this study was to test the hypothesis that preventive use of a soluble epoxide hydrolase inhibitor (sEHI) such as TPPU can decrease NSAID-induced ulcers by increasing anti-inflammatory epoxyeicosatrienoic acids (EETs). Dose-[10, 30, and 100 mg/kg, by mouth (PO)] and time-dependent (6 and 18 hours) ulcerative effects of diclofenac sodium (DCF, an NSAID) were studied in the small intestine of Swiss Webster mice. Dose-dependent effects of TPPU (0.001-0.1 mg/kg per day for 7 days, in drinking water) were evaluated in DCF-induced intestinal toxicity and compared with OME (20 mg/kg, PO). In addition, the effect of treatment was studied on levels of Hb in blood, EETs in plasma, inflammatory markers such as myeloperoxidase (MPO) in intestinal tissue homogenates, and tissue necrosis factor-a (TNF-a) in serum. DCF dose dependently induced ulcers that were associated with both a significant (P , 0.05) loss of Hb and an increase in the level of MPO and TNF-a, with severity of ulceration highest at 18 hours. Pretreatment with TPPU dose dependently prevented ulcer formation by DCF, increased the levels of epoxy fatty acids, including EETs, and TPPU's efficacy was comparable to OME. TPPU significantly (P , 0.05) reversed the effect of DCF on the level of Hb, MPO, and TNF-a. Thus sEHI might be useful in the management of NSAID-induced ulcers.

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“…Although a recent systematic review does not allow firm recommendations about the usefulness of n-3 PUFA dietary supplements in IBD (52), other works, especially at the preclinical stage, suggest that n-3 PUFAs or their lipid-derived mediators might have a therapeutic effect (19)(20)(21)53). Indeed, the n-3 PUFAs DHA and EPA, found in fish oils, are extensively used currently as dietary supplements and are thought to exert beneficial effects in a number of inflammationrelated diseases (54,55) and in different experimental models (53,56,57). More recently, EPA and DHA lipid-derived mediators known as resolvins and protectins have been described as key mediators in the resolution of inflammation and regulators of normal homeostasis (5,9).…”

Section: Discussionmentioning

confidence: 99%

Maresin 1, a Proresolving Lipid Mediator Derived from Omega-3 Polyunsaturated Fatty Acids, Exerts Protective Actions in Murine Models of Colitis

Marcon

Bento

Dutra

et al. 2013

The Journal of Immunology

173

149

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It has been previously reported that dietary fish oils, which are rich in the polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, can exert beneficial effects in inflammatory bowel disease. In this study, we investigated the effects of docosahexaenoic acid–derived lipid mediator maresin 1 (MaR1) in dextran sulfate sodium (DSS)– and 2,4,6-trinitrobenzenesulfonic acid–induced colitis in mice. Systemic treatment with MaR1 significantly attenuated both DSS- and 2,4,6-trinitrobenzene sulfonic acid–induced colonic inflammation by improving the disease activity index and reducing body weight loss and colonic tissue damage. MaR1 treatment also induced a significant decrease in levels of inflammatory mediators, such as IL-1β, TNF-α, IL-6, and IFN-γ, in the acute protocol, as well as IL-1β and IL-6, but not TNF-α and INF-γ, in the chronic DSS colitis protocol. Additionally, MaR1 decreased ICAM-1 mRNA expression in both the acute and chronic protocols of DSS-induced colitis. Furthermore, the beneficial effects of MaR1 seem to be associated with inhibition of the NF-κB pathway. Moreover, incubation of LPS-stimulated bone marrow–derived macrophage cultures with MaR1 reduced neutrophil migration and reactive oxygen species production, besides decreasing IL-1β, TNF-α, IL-6, and INF-γ production. Interestingly, macrophages incubated only with MaR1 showed a significant upregulation of mannose receptor C, type 1 mRNA expression, an M2 macrophage phenotype marker. These results indicate that MaR1 consistently protects mice against different models of experimental colitis, possibly by inhibiting the NF-κB pathway and consequently multiple inflammatory mediators, as well as by enhancing the macrophage M2 phenotype.

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Docosahexaenoic acid, an omega-3 polyunsaturated acid protects against indomethacin-induced gastric injury

Cited by 23 publications

References 20 publications

Gastrointestinal Bleeding After High Intake of Omega-3 Fatty Acids, Cortisone and Antibiotic Therapy: A Case Study

Gastrointestinal Bleeding After High Intake of Omega-3 Fatty Acids, Cortisone and Antibiotic Therapy: A Case Study

Anti-Ulcer Efficacy of Soluble Epoxide Hydrolase Inhibitor TPPU on Diclofenac-Induced Intestinal Ulcers

Maresin 1, a Proresolving Lipid Mediator Derived from Omega-3 Polyunsaturated Fatty Acids, Exerts Protective Actions in Murine Models of Colitis

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