NO and HNO donors, nitrones, and nitroxides: Past, present, and future

Oliveira, Catarina; Benfeito, Sofia; Fernandes, Carlos; Cagide, Fernando; Silva, Tiago

doi:10.1002/med.21461

Cited by 58 publications

(41 citation statements)

References 203 publications

(416 reference statements)

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“…Differences in metabolic mechanisms and following metabolites determine their pro‐inflammatory or anti‐inflammatory properties. M1 macrophages serve as the primary metabolizers of arginine to generate NO, promoting the development of inflammation . M2 macrophages (rodent) metabolize arginine to produce the anti‐inflammatory molecule ornithine.…”

Section: Activation and Proliferation Of Intestinal Mucosal Immune Cementioning

confidence: 99%

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Zhang

Reíter

et al. 2019

Medicinal Research Reviews

121

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Nowadays, melatonin, previously considered only as a pharmaceutical product for rhythm regulation and sleep aiding, has shown its potential as a co‐adjuvant treatment in intestinal diseases, however, its mechanism is still not very clear. A firm connection between melatonin at a physiologically relevant concentration and the gut microbiota and inflammation has recently established. Herein, we summarize their crosstalk and focus on four novelties. First, how melatonin is synthesized and degraded in the gut and exerts potentially diverse phenotypic effects through its diverse metabolites. Second, how melatonin mediates the activation and proliferation of intestinal mucosal immune cells with paracrine and autocrine properties. By modulating T/B cells, mast cells, macrophages and dendritic cells, melatonin immunomodulatory involved in regulating T‐cell differentiation, intervening T/B cell interaction and attenuating the production of pro‐inflammatory factors, achieving its antioxidant action via specific receptors. Third, how melatonin exerts antimicrobial action and modulates microbial components, such as lipopolysaccharide, amyloid‐β peptides via nuclear factor κ‐light‐chain‐enhancer of activated B cells (NF‐κB) or signal transducers and activators of transcription (STAT1) pathway to modulate intestinal immune function in immune‐pineal axis. The last, how melatonin mediates the effect of intestinal bacterial activity signals on the body rhythm system through the NF‐κB pathway and influences the mucosal epithelium oscillation via clock gene expression. These processes are achieved at mitochondrial and nuclear levels to control the host immune cell development. Considering unclear mechanisms and undiscovered actions of melatonin in gut‐microbiome‐immune axis, it's time to reveal them and provide new insight for the outlook of melatonin as a potential therapeutic target in the treatment and management of intestinal diseases.

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Section: Activation and Proliferation Of Intestinal Mucosal Immune Cementioning

confidence: 99%

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Zhang

Reíter

et al. 2019

Medicinal Research Reviews

121

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“…Nitric oxide, •N〓O (abbreviated as NO) is a diatomic molecule with an unpaired electron in its outer orbit. NO is a highly diffusible gaseous molecule, which easily crosses cell membranes due to its high lipophilicity [22]. NO is involved in different metabolic pathways.…”

Section: No and No Donorsmentioning

confidence: 99%

“…•− ) to produce nitrogen reactive species, including peroxynitrite [22][23][24]. At a cellular level, NO is a signaling molecule that regulates important processes such as cell differentiation and death, immune response, vascular tone and function, platelet aggregation, angiogenesis, and neurotransmission [25][26][27].…”

Section: No and No Donorsmentioning

confidence: 99%

Targeting the NO/cGMP/CREB Phosphorylation Signaling Pathway in Alzheimer’s Disease

Fiorito¹,

Deng²,

Landry³

et al. 2019

Neurochemical Basis of Brain Function and Dysfunction

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Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common form of senile dementia. Recently, scientists have put significant effort into exploring the molecular mechanisms involved in the pathological processes leading to the disease. A vast number of studies have focused on understanding the nitric oxide (NO) signaling pathway, which culminates with the phosphorylation of the transcription factor cAMP-responsive element-binding protein (CREB) through the increase of the second messenger cyclic guanosine monophosphate (cGMP) and activation of cGMP-dependent protein kinase. This book chapter provides an overview of the progress being made in modulating the hippocampal synaptic transmissions, which are critical for learning and memory, by targeting the different components of the NO/cGMP/CREB phosphorylation signaling pathway. Furthermore, a description of recent research on this pathway through the use of phosphodiesterase inhibitors is emphasized.

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“…prevention of stroke-induced mortality in models of ischemia in gerbils [103,104,[109][110][111][112][113]. The pharmacological effects of PBN in animal models are extensive, protecting against death after endotoxic shock, bacterial meningitis, teratogenicity induced by thalidomide, diabetogenesis, hepatocarcinogenesis, etc.…”

Section: Spin Trappingsmentioning

confidence: 99%

Current Developments in Antioxidant Therapies for Spinal Cord Injury

Villa¹,

Villamar²,

Zapien³

et al. 2019

Spinal Cord Injury Therapy [Working Title]

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When spinal cord injury (SCI) occurs, numerous sources of reactive oxygen species and nitrogen species may be active within first minutes or hours and even reactivate few days later. Free radical formation and lipid peroxidation (LP) have been described as an important mechanism in the beginning and accelerated progress in the development of diverse pathologies, importantly in those related to central nervous system. The compromise of molecules and cellular structures due to the oxidative state of microenvironment in SCI may determinate survival or apoptosis of resident and infiltrating cells and polarization toward an inflammatory response, which lead to an extension of damaged tissue and loss of neuronal function, or a regulatory/regenerative response. The investigation of new antioxidant agents and their action at a molecular level begins to reveal mechanisms that, if correctly modulated, promise an improvement in recovery of functions with respect to conventional pharmacological therapies. In this chapter, we will review the general mechanisms of oxidative stress and lipid peroxidation, those antioxidant treatments in experimental development and clinical phase, as well as their achievements and limitations.

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NO and HNO donors, nitrones, and nitroxides: Past, present, and future

Cited by 58 publications

References 203 publications

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Targeting the NO/cGMP/CREB Phosphorylation Signaling Pathway in Alzheimer’s Disease

Current Developments in Antioxidant Therapies for Spinal Cord Injury

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