Lipoxins, resolvins, protectins, maresins and nitrolipids, and their clinical implications with specific reference to cancer: part I

Das, Undurti N.

doi:10.2217/clp.13.31

Cited by 30 publications

(37 citation statements)

References 179 publications

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“…The relative proportions of LCPUFAs in cell membranes, as well as cell type, are the primary factors that regulate the formation of some of these bioactive lipid metabolites. It is likely that eSS rats treated with ω-3 LCPUFAs may lead to the formation of some of these anti-inflammatory metabolites such as lipoxins, resolvins and protectins [28, 29]. This assumption is supported by our recent studies that showed that lipoxin A4, an anti-inflammatory product formed from AA has anti-diabetic actions in chemical-induced diabetic animal models [27].…”

Section: Resultsmentioning

confidence: 95%

“…The LCPUFAs derived from LA and ALA serve as precursors to several biologically active molecules such as prostaglandins (PGs), leukotrienes (LTs), thromboxanes (TXs), lipoxins (LXs), resolvins, protectins and endocannabinoids. These metabolites have potent pro-inflammatory or anti-inflammatory actions [28, 29]. The relative proportions of LCPUFAs in cell membranes, as well as cell type, are the primary factors that regulate the formation of some of these bioactive lipid metabolites.…”

Section: Resultsmentioning

confidence: 99%

“…It is generally believed that under normal physiological conditions a balance is maintained between pro- and anti-inflammatory products formed to maintain normal homeostasis and suppress the initiation of low-grade systemic chronic inflammation in DM [5, 43]. In this context, it is noteworthy that ω-3 LCPUFAs induce their anti-inflammatory effects by acting on the GPR120 and Toll-like receptors (TLRs) [5, 28, 29, 36–38, 42, 43] that results in the suppression of formation of TNF-α and other pro-inflammatory cytokines especially in macrophages, adipocytes and hepatocytes [5, 28, 29, 43]. As a result, pro-inflammatory events are switched off or suppressed.…”

Section: Resultsmentioning

confidence: 99%

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Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

et al. 2016

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BackgroundDiabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.MethodsAfter weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%–6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.ResultsPlasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.ConclusionseSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

et al. 2016

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“…Despite these impressive results and arguments, it is noteworthy that the exact mechanism(s) by which EPA and DHA can prevent AAA induced by angiotensin-II infusion remains unclear. It is not clear whether EPA and DHA themselves can bring about this beneficial action or they need to be converted to their respective anti-inflammatory compounds such as resolvins and protectins and maresins [3][4][5][6] (resolvins E1, E2 and E3 are formed from EPA; while resolvins D1, D2, D3 and D4, protectins and maresins are formed from DHA, see Figures 1 and 2). Another important information that should have been generated is to know how much of the administered EPA and DHA were incorporated at the site of AAA and whether there is any correlation between the amount of EPA and DHA present and AAA.…”

Section: Pufas and Their Metabolites Angiotensin-ii Aa And Aaamentioning

confidence: 99%

“…Resolvins/protectins/maresins are not only antiinflammatory, [3][4][5][6] but also possess anti-fibrotic actions [15] and inhibit the proliferation of fibroblasts [15] and thus, angiotensin-II-induced AAA could be prevented. Since angiotensin-II has pro-inflammatory actions [11][12][13] and resolvins, protectins and maresins are anti-inflammatory in nature, this may explain the ability of EPA and DHA to prevent AAA.…”

Section: Pufas and Their Metabolites Angiotensin-ii Aa And Aaamentioning

confidence: 99%

Is aortic aneurysm preventable?

Das¹

2017

Journal of Translational Internal Medicine

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Abdominal aortic aneurysm (AAA) is a chronic inflammatory condition, triggered by the local accumulation of macrophages, oxidative stress and damage to the aortic wall. Pro-inflammatory eicosanoids seem to play a significant role in AAA. The pro-inflammatory events seen in AAA could be due to a deficiency of anti-inflammatory eicosanoids such as lipoxin A4 (LXA4), resolvins, protectins and maresins as a result of reduced tissue concentrations of their precursors: arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Thus, an imbalance between pro- and anti-inflammatory eicosanoids may underlie AAA. Angiotensin-II (Ang-II), a pro-inflammatory molecule, seems to have a role in AAA. I propose that AAA is due to the local (abdominal aortic wall) deficiency of AA and other PUFAs and their anti-inflammatory metabolites especially LXA4. The beneficial action of EPA and DHA reported in the animal experimental models of AAA induced by Ang-II infusion can be attributed to their (EPA and DHA) ability to enhance the formation of not only resolvins, protectins and maresins but also LXA4. It is likely that abdominal aortic tissue (endothelial cells, smooth muscle cells and other cells) may be deficient in AA, EPA and DHA, and have defective activity of 5-, 12-, and 15-lipoxygenases and cyclooxygenase, especially COX-2 resulting in decreased formation of LXA4, resolvins, protectins and maresins. Thus, methods designed to enhance the formation of LXA4 and other anti-inflammatory eicosanoids may form a new approach to prevent and manage AAA.

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Introduction to Genes, Oncogenes, and Anti-oncogenes

Das¹

2020

Molecular Biochemical Aspects of Cancer

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Lipoxins, resolvins, protectins, maresins and nitrolipids, and their clinical implications with specific reference to cancer: part I

Cited by 30 publications

References 179 publications

Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)

Is aortic aneurysm preventable?

Introduction to Genes, Oncogenes, and Anti-oncogenes

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