期刊
PROSTAGLANDINS & OTHER LIPID MEDIATORS
卷 136, 期 -, 页码 1-8出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2018.03.002
关键词
Leukotrienes; n-3 fatty acids; Myeloperoxidase; Specialised proresolving lipid mediators; Neutrophils
资金
- National Health and Medical Research Council of Australia [APP303151, APP1010495]
- Royal Perth Hospital Medical Research Foundation
- National Health and Medical Research Council of Australia
Background: Neutrophils release leukotriene (LT)B-4 and myeloperoxidase (MPO) that may be important mediators of chronic inflammation in chronic kidney disease (CKD). The n-3 fatty acids (n-3 FA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have the potential to attenuate inflammation through production of LTBs and the Specialized Proresolving Lipid Mediators (SPM) that promote the resolution of inflammation. In animal models, coenzyme Q10 (CoQ) also attenuates inflammation by reducing MPO and LTB4. Objective: This study evaluated the independent and combined effects of n-3 FA and CoQ supplementation on neutrophil leukotrienes, the pro-inflammatory eicosanoid 5-hydroxyeicosatetraenoic acid (5-HETE), SPM, and plasma MPO, in patients with CKD. Design: In a double-blind, placebo-controlled intervention of factorial design, 85 patients with CKD were randomized to either n-3 FA (4 g), CoQ (200 mg), both supplements, or control (4 g olive oil), daily for 8 weeks. Plasma MPO and calcium ionophore-stimulated neutrophil release of LTs, 5-HETE and SPM were measured at baseline and after 8 weeks. Results: Seventy four patients completed the intervention. n-3 FA, but not CoQ, significantly increased neutrophil LTBs (P < 0.0001) and the SPM 18-hydroxyeicosapentaenoic acid (18-HEPE), resolvin E1(RvE1), resolvin E2 (RvE2) and resolvin E3 (RvE3) that derive from EPA, as well as 17-hydroxydocosahexaenoic acid (17-HDHA) and resolvin D5 (RvD5) that derive from DHA (all P < 0.01). Neutrophil LTB4 and its metabolites, and 5-HETE were not significantly altered by n-3 FA or CoQ. Plasma MPO was significantly reduced with n-3 FA alone (P = 0.013) but not when given in combination with CoQ. Conclusion: n-3 FA supplementation in patients with CKD leads to increased neutrophil release of LTBs and several SPM, as well as a reduction in plasma MPO that may have important implications for limiting chronic inflammation.
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