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      Inflammation and cardiovascular disease: are marine phospholipids the answer?

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          Abstract

          This review presents the latest research on the cardioprotective effects of n-3 fatty acids (FA) and n-3 FA bound to polar lipids (PL). Overall, n-3 PL may have enhanced bioavailability and potentially bioactivity versus free FA and ester forms of n-3 FA.

          Abstract

          Since the discovery that Greenlandic Innuits had a lower risk of developing cardiovascular diseases (CVD) due to their diet of fish and as a consequence high polyunsaturated fatty acids (PUFA) intake, scientific interest in the therapeutic value of n-3 PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) has grown. It is well-accepted that fish consumption is associated with the prevention of inflammation and CVD. As a result, fish oil supplements and nutraceuticals are widely consumed. Conversely, recent meta-analyses have cast doubt over the benefits n-3 PUFA due to heterogenous outcomes of numerous randomized controlled trials. However, the majority of clinical studies conducted have used n-3 PUFA supplements in their neutral forms as free fatty acids or bound to triacylglycerides (TAG) or ethyl esters. Current research indicates that n-3 PUFA bound to polar lipids (PL) such as phospholipids seem to exert differential bioavailability and biological effects upon consumption in contrast to neutral forms of n-3 PUFA. In this review, we discuss the promising health benefits of marine PL rich in n-3 PUFA that seem to go beyond those of neutral n-3 PUFA. However, further intensive research is required to discern the full extent of the biological activities of marine n-3 PL and their potential use in functional foods and nutraceuticals.

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          Inflammation in atherosclerosis: from pathophysiology to practice.

          Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
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            Proresolving lipid mediators and mechanisms in the resolution of acute inflammation.

            Inflammatory responses, like all biological cascades, are shaped by a delicate balance between positive and negative feedback loops. It is now clear that in addition to positive and negative checkpoints, the inflammatory cascade rather unexpectedly boasts an additional checkpoint, a family of chemicals that actively promote resolution and tissue repair without compromising host defense. Indeed, the resolution phase of inflammation is just as actively orchestrated and carefully choreographed as its induction and inhibition. In this review, we explore the immunological consequences of omega-3-derived specialized proresolving mediators (SPMs) and discuss their place within what is currently understood of the role of the arachidonic acid-derived prostaglandins, lipoxins, and their natural C15-epimers. We propose that treatment of inflammation should not be restricted to the use of inhibitors of the acute cascade (antagonism) but broadened to take account of the enormous therapeutic potential of inducers (agonists) of the resolution phase of inflammation.
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              Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial.

              Large observational studies, small prospective studies and post-hoc analyses of randomised clinical trials have suggested that statins could be beneficial in patients with chronic heart failure. However, previous studies have been methodologically weak. We investigated the efficacy and safety of the statin rosuvastatin in patients with heart failure. We undertook a randomised, double-blind, placebo-controlled trial in 326 cardiology and 31 internal medicine centres in Italy. We enrolled patients aged 18 years or older with chronic heart failure of New York Heart Association class II-IV, irrespective of cause and left ventricular ejection fraction, and randomly assigned them to rosuvastatin 10 mg daily (n=2285) or placebo (n=2289) by a concealed, computerised telephone randomisation system. Patients were followed up for a median of 3.9 years (IQR 3.0-4.4). Primary endpoints were time to death, and time to death or admission to hospital for cardiovascular reasons. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00336336. We analysed all randomised patients. 657 (29%) patients died from any cause in the rosuvastatin group and 644 (28%) in the placebo group (adjusted hazard ratio [HR] 1.00 [95.5% CI 0.898-1.122], p=0.943). 1305 (57%) patients in the rosuvastatin group and 1283 (56%) in the placebo group died or were admitted to hospital for cardiovascular reasons (adjusted HR 1.01 [99% CI 0.908-1.112], p=0.903). In both groups, gastrointestinal disorders were the most frequent adverse reaction (34 [1%] rosuvastatin group vs 44 [2%] placebo group). Rosuvastatin 10 mg daily did not affect clinical outcomes in patients with chronic heart failure of any cause, in whom the drug was safe.
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                Author and article information

                Journal
                FFOUAI
                Food & Function
                Food Funct.
                Royal Society of Chemistry (RSC)
                2042-6496
                2042-650X
                April 30 2020
                2020
                : 11
                : 4
                : 2861-2885
                Affiliations
                [1 ]Department of Biological Sciences
                [2 ]University of Limerick
                [3 ]Limerick
                [4 ]Ireland
                [5 ]Health Research Institute (HRI)
                Article
                10.1039/C9FO01742A
                32270798
                f331bb98-46cf-44f9-8230-0eb7e5e06404
                © 2020

                http://rsc.li/journals-terms-of-use

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