Nitric oxide protected against NADPH oxidase-derived superoxide generation in vascular endothelium: Critical role for heme oxygenase-1

Luo, Mengjuan; Tian, Rong; Lu, Naihao

doi:10.1016/j.ijbiomac.2018.12.252

Cited by 19 publications

(15 citation statements)

References 29 publications

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“…The oxidant stress that can impair tight junction formation and maintenance in enterocytes often stems from NAD(P)H oxidase complexes (89,(104)(105)(106). The unconjugated bilirubin generated by heme oxygenase-mediated catabolism of heme functions as a direct inhibitor of such complexes (107)(108)(109)(110)(111). Unconjugated bilirubin has been found to improve intestinal barrier function in a rat model of ulcerative colitis, and to alleviate the loss of barrier functions associated with bile duct ligation (112,113).…”

Section: Antioxidants Can Aid Tight Junction Maintenance By Downregulating Mapk Activitymentioning

confidence: 99%

Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function

McCarty

Lerner

2021

Advances in Nutrition

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Impairment of intestinal barrier function is linked to certain pathologies and to aging, and can be a cause of bacterial infections, systemic and hepatic inflammation, food allergies, and autoimmune disorders. The formation and maintenance of intestinal tight junctions is supported by glucagon-like peptide-2 (GLP-2), which via insulin-like growth factor I activity boosts phosphoinositide 3-kinase/Akt/mammalian target of rapamycin complex 1 (PI3K/Akt/mTORC1) signaling in enterocytes. 5′-AMP-activated protein kinase (AMPK) activity as well as estrogen receptor-β (ERβ) activity are also protective in this regard. Conversely, activation of mitogen-activated protein kinases (MAPKs) and cellular Src (c-Src) under inflammatory conditions can induce dissociation of tight junctions. Hence, nutraceuticals that promote GLP-2 secretion from L cells—effective pre/probiotics, glycine, and glutamine—as well as diets rich in soluble fiber or resistant starch, can support intestinal barrier function. AMPK activators—notably berberine and the butyric acid produced by health-promoting microflora—are also beneficial in this regard, as are soy isoflavones, which function as selective agonists for ERβ. The adverse impact of MAPK and c-Src overactivation on the intestinal barrier can be combatted with various antioxidant measures, including phycocyanobilin, phase 2–inducer nutraceuticals, and N-acetylcysteine. These considerations suggest that rationally designed functional foods or complex supplementation programs could have clinical potential for supporting and restoring healthful intestinal barrier function.

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Section: Antioxidants Can Aid Tight Junction Maintenance By Downregulating Mapk Activitymentioning

confidence: 99%

Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function

McCarty

Lerner

2021

Advances in Nutrition

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“…NO has an important protective effect on maintaining normal cardiovascular function. Excessive ROS production can reduce the bioavailability of NO, which is the main factor for the occurrence and development of CVDs [49]. For example, the activation of NF-κB after radiation is inhibited 4 Oxidative Medicine and Cellular Longevity by NO, and therefore, a decrease in the bioavailability of NO may promote the development of vascular inflammation and atherosclerosis [40].…”

Section: Igf-1 and Oxidative Stressmentioning

confidence: 99%

Oxidative Stress in Radiation-Induced Cardiotoxicity

Zhang

Yang

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

115

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There is a distinct increase in the risk of heart disease in people exposed to ionizing radiation (IR). Radiation-induced heart disease (RIHD) is one of the adverse side effects when people are exposed to ionizing radiation. IR may come from various forms, such as diagnostic imaging, radiotherapy for cancer treatment, nuclear disasters, and accidents. However, RIHD was mainly observed after radiotherapy for chest malignant tumors, especially left breast cancer. Radiation therapy (RT) has become one of the main ways to treat all kinds of cancer, which is used to reduce the recurrence of cancer and improve the survival rate of patients. The potential cause of radiation-induced cardiotoxicity is unclear, but it may be relevant to oxidative stress. Oxidative stress, an accumulation of reactive oxygen species (ROS), disrupts intracellular homeostasis through chemical modification and damages proteins, lipids, and DNA; therefore, it results in a series of related pathophysiological changes. The purpose of this review was to summarise the studies of oxidative stress in radiotherapy-induced cardiotoxicity and provide prevention and treatment methods to reduce cardiac damage.

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“…Moreover, oxidants generated by these complexes often play a co-factor role in signaling pathways that activate NF-kappaB, possibly by expediting the assembly of certain protein signaling complexes [119,120]. The enzyme heme oxygenase-1 (HO-1) exerts its antioxidant effects in large part by generating intracellular free bilirubin via degradation of free heme; bilirubin has been shown to inhibit certain NADPH oxidase complexes in physiological intracellular concentrations [121][122][123][124][125][126]. Although the isoform specificity of this effect has not yet been adequately explored, NOX2 and NOX4 appear to be susceptible to bilirubin-mediated inhibition.…”

Section: Controlling Oxidative Stress With Phycocyanobilinmentioning

confidence: 99%

Nutraceutical Strategies for Suppressing NLRP3 Inflammasome Activation: Pertinence to the Management of COVID-19 and Beyond

et al. 2020

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Inflammasomes are intracellular protein complexes that form in response to a variety of stress signals and that serve to catalyze the proteolytic conversion of pro-interleukin-1β and pro-interleukin-18 to active interleukin-1β and interleukin-18, central mediators of the inflammatory response; inflammasomes can also promote a type of cell death known as pyroptosis. The NLRP3 inflammasome has received the most study and plays an important pathogenic role in a vast range of pathologies associated with inflammation—including atherosclerosis, myocardial infarction, the complications of diabetes, neurological and autoimmune disorders, dry macular degeneration, gout, and the cytokine storm phase of COVID-19. A consideration of the molecular biology underlying inflammasome priming and activation enables the prediction that a range of nutraceuticals may have clinical potential for suppressing inflammasome activity—antioxidants including phycocyanobilin, phase 2 inducers, melatonin, and N-acetylcysteine, the AMPK activator berberine, glucosamine, zinc, and various nutraceuticals that support generation of hydrogen sulfide. Complex nutraceuticals or functional foods featuring a number of these agents may find utility in the prevention and control of a wide range of medical disorders.

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Nitric oxide protected against NADPH oxidase-derived superoxide generation in vascular endothelium: Critical role for heme oxygenase-1

Cited by 19 publications

References 29 publications

Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function

Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function

Oxidative Stress in Radiation-Induced Cardiotoxicity

Nutraceutical Strategies for Suppressing NLRP3 Inflammasome Activation: Pertinence to the Management of COVID-19 and Beyond

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