The nitric oxide donor cis-[Ru(bpy)2(SO3)NO](PF6) increases gastric mucosa protection in mice – Involvement of the soluble guanylate cyclase/KATP pathway

Santana, Ana Paula M.; Tavares, Bruno de Melo; Lucetti, Larisse T.; Gouveia, Florêncio S.; Ribeiro, Ronaldo A.; Soares, Pedro Marcos Gomes; Sousa, Eduardo Henrique Silva; Lopes, Luiz Gonzaga de França; Medeiros, Jand Venes R.; Souza, Marcellus H.

doi:10.1016/j.niox.2015.02.002

Cited by 29 publications

(11 citation statements)

References 34 publications

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“…NO generation can be stimulated by cytokines and NO donors [77,78]. NO affects cell survival, the immune response, insulin signaling, and stress disorders and provides vascular and neural protection [72,76,79,80,81,82,83,84].…”

Section: G6pd and Cellular Signaling With Emphasis On Redox Signalingmentioning

confidence: 99%

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Yang

Yen

et al. 2019

Cells

184

132

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The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

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Section: G6pd and Cellular Signaling With Emphasis On Redox Signalingmentioning

confidence: 99%

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Yang

Yen

et al. 2019

Cells

184

132

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“…In addition, NO is intimately involved in regulating all aspects of our lives from waking, digestion, sexual function, perception of pain and pleasure, memory recall and sleeping [40,41]. Moreover, NO is known to have a protective effect on the gastrointestinal tract (GT), based on its properties in stimulating gastric mucus secretion to increase the mucosal blood flow and to inhibit the leukocyte adherence to the vascular endothelium [39,42,43].…”

Section: Introductionmentioning

confidence: 99%

Design, Synthesis, In Silico and In Vitro Studies for New Nitric Oxide-Releasing Indomethacin Derivatives with 1,3,4-Oxadiazole-2-thiol Scaffold

Sava

Buron

Routier

et al. 2021

IJMS

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Starting from indomethacin (IND), one of the most prescribed non-steroidal anti-inflammatory drugs (NSAIDs), new nitric oxide-releasing indomethacin derivatives with 1,3,4-oxadiazole-2-thiol scaffold (NO-IND-OXDs, 8a-p) have been developed as a safer and more efficient multitarget therapeutic strategy. The successful synthesis of designed compounds (intermediaries and finals) was proved by complete spectroscopic analyses. In order to study the in silico interaction of NO-IND-OXDs with cyclooxygenase isoenzymes, a molecular docking study, using AutoDock 4.2.6 software, was performed. Moreover, their biological characterization, based on in vitro assays, in terms of thermal denaturation of serum proteins, antioxidant effects and the NO releasing capacity, was also performed. Based on docking results, 8k, 8l and 8m proved to be the best interaction for the COX-2 (cyclooxygense-2) target site, with an improved docking score compared with celecoxib. Referring to the thermal denaturation of serum proteins and antioxidant effects, all the tested compounds were more active than IND and aspirin, used as references. In addition, the compounds 8c, 8h, 8i, 8m, 8n and 8o showed increased capacity to release NO, which means they are safer in terms of gastrointestinal side effects.

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“…The ruthenium NO donors inhibit inflammatory pain behaviors induced by formalin and carrageenan by reducing the recruitment of neutrophils (Staurengo-Ferrari et al, 2013), cytokine production and oxidative stress in mice (Staurengo-Ferrari et al, 2014a), and activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway (Staurengo-Ferrari et al, 2013, 2014a). The nitric oxide donor cis -[Ru(bpy) 2 (SO 3 )NO](PF 6 ) has protective effect of the gastric mucosa against the damage caused by naproxen or ethanol in mice (Santana et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

[Ru(bpy)2(NO)SO3](PF6), a Nitric Oxide Donating Ruthenium Complex, Reduces Gout Arthritis in Mice

et al. 2019

Self Cite

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Monosodium urate crystals (MSU) deposition induces articular inflammation known as gout. This disease is characterized by intense articular inflammation and pain by mechanisms involving the activation of the transcription factor NFκB and inflammasome resulting in the production of cytokines and oxidative stress. Despite evidence that MSU induces iNOS expression, there is no evidence on the effect of nitric oxide (NO) donors in gout. Thus, the present study evaluated the effect of the ruthenium complex donor of NO {[Ru(bpy)2(NO)SO3](PF6)} (complex I) in gout arthritis. Complex I inhibited in a dose-dependent manner MSU-induced hypersensitivity to mechanical stimulation, edema and leukocyte recruitment. These effects were corroborated by a decrease of histological inflammation score and recruitment of Lysm-eGFP+ cells. Mechanistically, complex I inhibited MSU-induced mechanical hypersensitivity and joint edema by triggering the cGMP/PKG/ATP-sensitive K (+) channels signaling pathway. Complex I inhibited MSU-induced oxidative stress and pro-inflammatory cytokine production in the knee joint. These data were supported by the observation that complex I inhibited MSU-induced NFκB activation, and IL-1β expression and production. Complex I also inhibited MSU-induced activation of pro-IL-1β processing. Concluding, the present data, to our knowledge, is the first evidence that a NO donating ruthenium complex inhibits MSU-induced articular inflammation and pain. Further, complex I targets the main physiopathological mechanisms of gout arthritis. Therefore, it is envisaged that complex I and other NO donors have therapeutic potential that deserves further investigation.

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The nitric oxide donor cis-[Ru(bpy)2(SO3)NO](PF6) increases gastric mucosa protection in mice – Involvement of the soluble guanylate cyclase/KATP pathway

Cited by 29 publications

References 34 publications

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Design, Synthesis, In Silico and In Vitro Studies for New Nitric Oxide-Releasing Indomethacin Derivatives with 1,3,4-Oxadiazole-2-thiol Scaffold

[Ru(bpy)2(NO)SO3](PF6), a Nitric Oxide Donating Ruthenium Complex, Reduces Gout Arthritis in Mice

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