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Anti-Inflammatory Compounds Derived from Marine Macroalgae
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Snezana Agatonovic-Kustrin, David W. Morton
Increasing attention has been paid to the anti-inflammatory activity of phlorotannins from seaweeds, especially from the Eisenia and Ecklonia genera due to their wide distribution and ecological importance (Bolton 2010). These compounds have the ability to down-regulate inducible nitric oxide synthase (iNOS) expression in cells exposed to lipopolysaccharide (LPS), thus exerting an anti-inflammatory action by the reduction of nitric oxide (NO) production. Nitric oxide is an important biological mediator, a signaling molecule that plays a key role in the pathogenesis of inflammation. It gives an anti-inflammatory effect under normal physiological conditions (Giles 2006). However, excessive production of NO, catalyzed by iNOS, is pathogenic for host tissues (Aktan 2004). Hence, inhibition of NO accumulation is a beneficial therapeutic strategy for the treatment of NO-mediated conditions. It is becoming evident that NO is also a major signaling molecule in plants and is involved in multiple plant physiological functions (Palavan-Unsal and Arisan 2009).
Thermal Physiology and Thermoregulation
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
Nitric oxide (NO) is a toxic, colorless, free-radical gas and one of the principal oxides of nitrogen. Inhaling a 100 ppm (120 mg/m3) concentration of nitric oxide can be dangerous to life and health.47 Within the human body, however, NO is a highly diffusible intercellular signaling molecule involved in a wide range of biological effects. It is one of the smallest molecules involved in intercellular signaling. The gas is highly reactive and short-lived, with a half-life of only a few seconds, yet it diffuses freely across biological membranes.48 These attributes make NO an ideal transient signaling molecule for events such as vasorelaxation and neurotransmission. Once converted to nitrites or nitrates by reaction with oxygen and water, the signaling activity of NO ceases.
The Arteries, the Endothelium, Endothelial Dysfunction, Glycocalyx, Glycocalyx Dysfunction, Nitric Oxide, and CHD
Published in Mark C Houston, The Truth About Heart Disease, 2023
The endothelium acts like an endocrine organ which makes numerous compounds that regulate blood pressure, vascular inflammation, oxidative stress, immune function, and risk of clotting and growth in the heart muscle and arteries. The functions determine future CHD, MI, and overall arterial health. One of these compounds is nitric oxide, which helps to dilate the artery and lower blood pressure. Nitric oxide is a short-lived gas that also provides numerous other health benefits to the artery, reducing blood pressure and the risk of CHD. The endothelium must function normally to prevent CHD (1–13). The endothelium is the largest organ in the body (2–5, 11–13). It is the size of six and a half tennis courts or about 14,000 square feet (2–5, 11–13).
The prevention and management strategies for neonatal chronic lung disease
Published in Expert Review of Respiratory Medicine, 2023
Christopher Harris, Anne Greenough
A Cochrane review of inhaled nitric oxide use in preterm infants with respiratory failure examined three different timings of the intervention: early treatment (within 3 days) for impaired oxygenation (eight trials), routine use in infants requiring respiratory support (four trials), and later use in those at an increased risk of BPD (three trials) [70]. No benefits to receiving iNO were seen regarding any of the timings of iNO administration. There were, however, trends toward positive outcomes, and it could be argued that more select entry criteria to better define a high-risk population might result in more positive results. A trial of 800 infants born between 24 and 28 + 6 weeks of gestational age included those with mild disease, that is requiring surfactant or CPAP for RDS within the first 24 hours of birth. They were randomized to inhaled nitric oxide (iNO) or placebo at 5 ppm for a minimum of 7 days and a maximum of 21 days. No significant differences were found in BPD development or death [71]. At 7-year follow-up, rates of rehospitalisation and use of respiratory medications were similar between the two groups [72].
Effects of Citrulline Malate Supplementation on Muscle Strength in Resistance-Trained Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
Published in Journal of Dietary Supplements, 2022
Andreo F. Aguiar, Juliano Casonatto
Nitric oxide (NO)-stimulating nutritional supplements are commonly advertised and marketed between athletes and amateur practitioners engaged in high-intensity exercise programs (Bloomer 2010). NO is a gaseous molecule produced at high levels in skeletal muscle (Stamler and Meissner 2001) by neuronal nitric oxide synthase (nNOS) that catalyzes the conversion of L-arginine to L-citrulline and generates the NO (Ckless et al. 2007). The main physiological effect of NO related to physical exercise is vasodilation (Joyner and Dietz 1997; Simmonds et al. 2014) and consequent increases the supply of oxygen and energy substrates to the active muscles (Joyner and Casey 2015), but it also acts in other physiological processes, including mitochondrial respiration (Poderoso et al. 2019), release of calcium from the sarcoplasmic reticulum (Heunks et al. 2001), muscle regeneration and hypertrophy (Smith et al. 2002; Aguiar et al. 2017), glucose uptake (Higaki et al. 2001; Hong et al. 2014), and muscle fatigue (Percival et al. 2010). Given these multiple physiological effects, NO-stimulating dietary supplements (e.g., citrulline and arginine) have been advocated to increase performance in high-intensity exercises (Bailey et al. 2015; Viribay et al. 2020).
Management of acute chest syndrome in patients with sickle cell disease: a systematic review of randomized clinical trials
Published in Expert Review of Hematology, 2022
Muhammad Rafay Khan Niazi, Divya Chukkalore, Abdullah Jahangir, Syeda Sahra, Kira Macdougall, Maryam Rehan, Marcel Odaimi
Maitre et al. [35] studied the effect of inhaled nitric oxide (80 ppm) in patients with ACS on length of hospital stay (LOS) and rate of treatment failure. Treatment failure was defined as any one of the following: (1) death from any cause, (2) need for endotracheal intubation, (3) decrease of PaO2/FiO2 ≥ 15 mmHg between days 1 and 3, (4) augmented therapy defined as new transfusion or phlebotomy. Rate of treatment failure was found to be similar between inhaled nitric oxide (N = 50) and placebo groups (N = 50), (23 [46%] and 29 [58%]; odds ratio [OR], 0.8; 95% CI, 0.54–1.16; p = 0.23). Post-hoc analysis of 45 hypoxemic patients showed lower treatment failure rate on day 3 in inhaled nitric oxide group as compared to the placebo group: (7 [33.3%] vs 18 [72%]; [OR], 0.19; 95% CI, 0.06–0.68; p = 0.009]. Gladwin et al. [36] also investigated the effect of inhaled nitric oxide in patients (>10 years of age). The incidence of ACS in both the groups was found to be similar 8 (10.7% [4.7–19.9]) vs placebo 7(9.3% [3.8–18.3%] p = 0.79).