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The Beneficial Effect of Omega-3 PUFA and L-Arginine on Endothelial Nitric Oxide (NO) Bioavailability
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
Endothelial NO also controls the expression of genes involved in atherogenesis. NO decreases the expression of chemoattractant protein MCP-1 and of a number of surface adhesion molecules, thereby preventing leucocyte adhesion to vascular endothelium and leucocyte migration into the vascular wall. This offers protection against early phases of atherogenesis. Also, the decreased endothelial permeability, the reduced influx of lipoproteins into the vascular wall and the inhibition of low-density lipoprotein oxidation may contribute to the anti-atherogenic properties of endothelial NOS-derived NO.
Embryology, Anatomy, and Physiology of the Male Reproductive System
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Smaller amount of NO is released from the endothelium via endothelial NOS (eNOS).L-citrulline + O2 → NO
Subfamily Bombacoideae
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Mariam I. Gamal El-Din, Fadia S. Youssef, Mohamed L. Ashour, Omayma A. Eldahshan, Abdel Nasser B. Singab
Nitric oxide (NO) is a signaling molecule playing a crucial role in the pathogenesis of inflammation. NO is generated biochemically through the oxidation of the terminal guanidine nitrogen atom from L-arginine by nitric oxide synthetase (NOS). Having three isoforms, endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS), nitric oxide synthase is an important cellular mediator of both physiological and pathological inflammatory processes. Endothelial NOS (eNOS) and neuronal NOS (nNOS) are constitutively expressed in the body under normal physiological conditions. However, inducible NOS (iNOS) is an inducible enzyme highly expressed by inflammatory stimuli. Overproduction of NO by inducible NOS occurs in response to different inflammatory mediators (e.g., tumor necrosis factor-α (TNF-α), interleukine-1β (IL-1β), and bacterial lipopolysaccharide (LPS)), aggravating the inflammatory process and acting synergistically with other inflammatory mediators. Many plants have recently proved to possess strong inhibitory potential of inducible NOS enzyme (iNOS), inhibiting overproduction of nitric oxide.
(E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone isolated from Portulaca oleracea L. suppresses LPS-induced inflammation in RAW 264.7 macrophages by downregulating inflammatory factors
Published in Immunopharmacology and Immunotoxicology, 2021
Eunji Kang, Jae Eun Park, Youngwan Seo, Ji Sook Han
Studies have shown that NOS synthesizes NO as a by-product while converting L-arginine to L-citrulline, which is significantly expressed by iNOS [8,32]. There are three isotypes of NOS: neuronal NOS (nNOS), endothelial NOS (eNOS) and iNOS. Under normal conditions, cells typically do not express iNOS. However, iNOS has been reported to be induced on expression of stimuli such as LPS, cytokines, or NF-κB, and thereby, generate large amounts of NO [33,34]. Subsequently, NO has been shown to mediate inflammatory response by interacting with superoxide anion to form a toxic oxidant peroxynitrite (ONOO-), which then activates macrophages [35]. This reaction has been observed to promote excessive inflammatory response by further increasing the expression of other inflammatory mediators [33]. In this study, exposure to LPS upregulated NO expression level, while HM-chromanone treatment was observed to significantly restore NO production. This suggested that HM-chromanone can suppress LPS-induced inflammatory response. Similarly, brazilin, a homoisoflavonoid compound, has been reported to inhibit NO production in LPS-activated RAW 264.7 macrophages by inhibiting iNOS at mRNA and protein level [36]. Another study has shown that 4′-O-demethylophiopogonanone E, which is a homoisoflavonoid compound from Ophiopogon japonicas, also lowers NO production, and is associated with suppression of iNOS expression in LPS-induced RAW 264.7 macrophages [37].
Emerging drugs for the prevention of migraine
Published in Expert Opinion on Emerging Drugs, 2021
Oyindamola Ogunlaja, Nazia Karsan, Peter Goadsby
Nitric oxide (NO) is a gaseous molecule that is involved in a range of physiological processes in the human body. Endogenous NO is produced by the oxidation of L-arginine to produce L-citrulline and NO [99]. This reaction is catalyzed by nitric oxide synthase (NOS), of which there are three isoforms. These isoforms are named after the tissue in which they were discovered and are predominantly expressed [99]. Neuronal NOS (nNOS) is expressed in neurons and is found in the central and peripheral nervous system [100]. Endothelial NOS (eNOS) was initially discovered in the vascular endothelium but is also found in platelets, cardiomyocytes, and the brain [100]. Inducible NOS (iNOS) is the final form that is found in macrophages, glial cells, and neurons. Unlike the first two, it is not constitutively active but is induced by infection and proinflammatory cytokines [99–101].
Angiotensin II type 1 receptor autoantibody blockade improves cerebral blood flow autoregulation and hypertension in a preclinical model of preeclampsia
Published in Hypertension in Pregnancy, 2020
Jeremy W. Duncan, Daniel Azubuike, George W. Booz, Brandon Fisher, Jan M. Williams, Fan Fan, Tarek Ibrahim, Babbette LaMarca, Mark W. Cunningham
NO bioavailability and oxidative stress can critically alter cerebral health and brain injury outcomes (36–38). Oxidative stress, endothelial dysfunction, and a reduction in NO bioavailability is a key mediator of cerebrovascular dysfunction in diverse forms of disease and aging, and of endothelial protection against BBB breakdown(39). In this study, we show that activated eNOS is increased in placental ischemic rats treated with “n7AAc,” indicating that AT1-AA inhibition could enhance the availability of NO and provide neuroprotection from cerebrovascular dysfunction(40). The increase in NO bioavailability may also contribute to protection of CBF autoregulation in the brain. Multiple studies have shown that NO plays a critical role in maintaining blood flow despite changes in systemic pressure in both humans and animals (41–43). Studies performed in rodents using nonspecific NOS inhibitors (such as L-NMA) impaired CBF at lower blood pressures, due to the inability of cerebrovessels to dilate in response to decreases in pressure(42). However, specific neuronal (n) NOS inhibitors (such as 7-nitro indazole) did not alter pressure-induced changes in CBF or vessel diameter, suggesting that NO derived from endothelial NOS (eNOS), and not neuronal NOS (nNOS), plays a major role in regulating CBF. This is consistent with our finding that phospho-eNOS protein increased with “n7AAc” RUPP treated rats, suggesting that AT1-AA inhibition could potentially improve CBF responses due to increases in phospho-eNOS-mediated cerebral NO (41,42).