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1.
Mar Drugs ; 20(7)2022 Jul 01.
Article in English | MEDLINE | ID: mdl-35877734

ABSTRACT

Lipid peroxidation is associated with the development of some pathologies, such as cardiovascular diseases. Reduction in oxidative stress by antioxidants, such as Arthrospira (formely Spirulina), helps improving this redox imbalance. The aim of the study was to evaluate the effect of the Arthrospira liquid extract "Spirulysat®" on oxidative markers-in particular, oxidized LDL (oxLDL)/total LDL cholesterol-and isoprostanes and to investigate its impact on lipid and glucose metabolism in the metabolic syndrome subject. A controlled, randomised, double-blind design was conducted in 40 subjects aged 18 to 65 years with metabolic syndrome after a daily intake of Spirulysat® or placebo for twelve weeks. Blood and urinary samples were collected at three visits (V1, V2, V3) in the two groups for parameters determination. Although the Spirulysat® group showed a decrease at all visits of the oxLDL/total cholesterol ratio, there was no significant difference compared to the placebo (p = 0.36). The urinary isoprostanes concentration in the Spirulysat® group was reduced (p = 0.014) at V3. Plasma triglycerides decreased at V3 (p = 0.003) and HDL-cholesterol increased (p = 0.031) at all visits with Spirulysat®. In conclusion, Spirulysat® did not change the oxidized LDL (oxLDL)/LDL ratio but decreased the urinary isoprostanes, plasma triglycerides and increased HDL cholesterol, suggesting a beneficial effect on metabolic syndrome.


Subject(s)
Metabolic Syndrome , Spirulina , Antioxidants/pharmacology , Antioxidants/therapeutic use , Cholesterol , Cholesterol, HDL , Double-Blind Method , Humans , Isoprostanes/pharmacology , Isoprostanes/therapeutic use , Lipoproteins, LDL , Metabolic Syndrome/drug therapy , Oxidative Stress , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Triglycerides
2.
Mol Aspects Med ; 64: 161-168, 2018 12.
Article in English | MEDLINE | ID: mdl-29572110

ABSTRACT

ω3 Polyunsaturated fatty acids (ω3 PUFAs) have several biological properties including anti-arrhythmic effects. However, there are some evidences that it is not solely ω3 PUFAs per se that are biologically active but the non-enzymatic oxygenated metabolites of polyunsaturated fatty acids (NEO-PUFAs) like isoprostanes and neuroprostanes. Recent question arises how these molecules take part in physiological homeostasis, show biological bioactivities and anti-inflammatory properties. Furthermore, they are involved in the circulations of childbirth, by inducing the closure of the ductus arteriosus. In addition, oxidative stress which can be beneficial for the heart in given environmental conditions such as the presence of ω3 PUFAs on the site of the stress and the signaling pathways involved are also explained in this review.


Subject(s)
Arrhythmias, Cardiac/drug therapy , Fatty Acids, Omega-3/metabolism , Isoprostanes/metabolism , Neuroprostanes/metabolism , Anti-Asthmatic Agents/therapeutic use , Arrhythmias, Cardiac/pathology , Ductus Arteriosus/drug effects , Ductus Arteriosus/metabolism , Fatty Acids, Omega-3/therapeutic use , Humans , Inflammation/drug therapy , Inflammation/pathology , Isoprostanes/therapeutic use , Neuroprostanes/therapeutic use , Oxidative Stress/drug effects , Signal Transduction/drug effects
3.
J Hypertens ; 28(2): 201-12, 2010 Feb.
Article in English | MEDLINE | ID: mdl-20051913

ABSTRACT

Pulmonary arterial hypertension (PAH) is a chronic and progressive disease characterized by a persistent elevation of pulmonary artery pressure accompanied by right ventricular hypertrophy (RVH). The current treatment for pulmonary hypertension is limited and only provides symptomatic relief due to unknown cause and pathogenesis of the disease. Both vasoconstriction and structural remodeling (enhanced proliferation of vascular smooth muscle cell) of the pulmonary arteries contribute to the progressive course of PAH, irrespective of different underlying causes. The exact molecular mechanism of PAH, however, is not fully understood. The purpose of this review is to provide recent advances in the mechanistic investigation of PAH. Specifically, this review focuses on nitric oxide, oxidative stress and inflammation and how these factors contribute to the development and progression of PAH. This review also discusses recent and potential therapeutic advancements for the treatment of PAH.


Subject(s)
Hypertension, Pulmonary/etiology , Hypertension, Pulmonary/physiopathology , Nitric Oxide/physiology , Animals , Chemokines/physiology , Cytokines/physiology , Endothelin Receptor Antagonists , Humans , Hypertension, Pulmonary/drug therapy , Inflammation/physiopathology , Isoprostanes/therapeutic use , Models, Biological , Nitric Oxide/therapeutic use , Oxidative Stress , Phosphodiesterase Inhibitors/therapeutic use , Pulmonary Artery/pathology , Pulmonary Artery/physiopathology , Reactive Oxygen Species/metabolism
4.
J Glaucoma ; 10(3): 215-9, 2001 Jun.
Article in English | MEDLINE | ID: mdl-11442186

ABSTRACT

PURPOSE: To compare the effect of pilocarpine, an agent that reduces uveoscleral outflow, on the ocular hypotensive efficacy of latanoprost and 8-iso prostaglandin E2 (PGE2). METHODS: Each of the two treatment groups was composed of the same eight monkeys with unilateral laser-induced glaucoma. Intraocular pressure (IOP) was measured hourly for 6 hours beginning at 9:00 AM on the baseline day (Thursday before treatment week) and on treatment days 1, 3, and 5 (Monday, Wednesday, and Friday). On all five treatment days, one drop of pilocarpine 4% was administered at 9:00 AM and 3:00 PM and one drop of latanoprost 0.005% or 25 microL of 8-iso PGE2 0.1% was administered at 10:00 AM and 4:00 PM. RESULTS: One hour after pilocarpine instillation on day 1, the reduction of IOP was similar (P > 0.90) in both treatment groups, 7.6 +/- 1.1 mm Hg (mean +/- standard error of the mean ) in the latanoprost group and 7.4 +/- 0.8 mm Hg in the 8-iso PGE2 group. However, the IOP effects of the two treatment groups became significantly different (P < 0.05) beginning 2 hours after dosing with latanoprost or 8-iso PGE, on day 1. A difference (P < 0.05) between the two groups persisted at all subsequent measurements. The reduction of IOP lessened with repeated dosing in the latanoprost and 8-iso PGE2 groups. Three hours after dosing with pilocarpine and two hours after dosing with the prostanoids, the IOP reduction was 8.3 +/- 0.9 mm Hg in the latanoprost group and 9.9 +/- 0.6 mm Hg in the 8-iso PGE2 group on day 1, and 2.1 +/- 1.0 mm Hg in the latanoprost group and 7.3 +/- 0.9 mm Hg in the 8-iso PGE1 group on day 5. CONCLUSIONS: The smaller reductions in IOP with pilocarpine and latanoprost than with pilocarpine and 8-iso PGE2 show that pilocarpine blocks much more of the ocular hypotensive effect of latanoprost than of 8-iso PGE2. The results also indicate that pilocarpine and latanoprost are mutually antagonistic. Enhancement of uveoscleral outflow appears to account for most of the ocular hypotensive effect of latanoprost and for much less of the ocular hypotensive effect of 8-iso prostaglandin E2.


Subject(s)
Antihypertensive Agents/therapeutic use , Dinoprostone/therapeutic use , Glaucoma/drug therapy , Intraocular Pressure/drug effects , Isoprostanes/therapeutic use , Pilocarpine/therapeutic use , Prostaglandins F, Synthetic/therapeutic use , Administration, Topical , Animals , Antihypertensive Agents/administration & dosage , Dinoprostone/administration & dosage , Dinoprostone/analogs & derivatives , Drug Therapy, Combination , Female , Glaucoma/etiology , Isoprostanes/administration & dosage , Laser Coagulation , Latanoprost , Macaca fascicularis , Ophthalmic Solutions , Pilocarpine/administration & dosage , Prostaglandins F, Synthetic/administration & dosage , Tonometry, Ocular , Trabecular Meshwork/surgery
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