The ruthenium nitric oxide donor, [Ru(HEDTA)NO], inhibits acute nociception in mice by modulating oxidative stress, cytokine production and activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway

Staurengo‐Ferrari, Larissa; Mizokami, Sandra S.; Fattori, Victor; Silva, Jean J.; Zanichelli, Patrícia Graça; Georgetti, Sandra R.; Baracat, Marcela M.; França, Luiz G. da; Pavanelli, Wander Rogério; Casagrande, Rúbia; Verri, Waldiceu A.

doi:10.1007/s00210-014-1030-0

Cited by 11 publications

(4 citation statements)

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“…Therefore, modulating oxidative stress is a conceivable approach to diminish pain and inflammation [55,56]. Curcumin presents prominent antioxidant activity and contributes to increasing GSH, catalase and SOD levels [57].…”

Section: •-mentioning

confidence: 99%

“…This cycle grants the neutralization of ROS and provides an antioxidant function to HO-1 [64]. Activation of cGMP/PKG/ATP-sensitive potassium channels lead to antinociceptive state [55,65]. Co-treatment with an HO-1 inducer increased the antinociceptive effects of opioids and cannabinoids through activation of cGMP/PKG/ATP-sensitive potassium channel pathway in a model of CFAinduced pain [66].…”

Section: •-mentioning

confidence: 99%

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Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-κB activation

et al. 2015

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Section: •-mentioning

confidence: 99%

Section: •-mentioning

confidence: 99%

Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-κB activation

et al. 2015

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“…Furthermore, oxidative stress causes tissue damage. In this sense, reducing oxidative stress diminishes disease severity (Del Carlo and Loeser, 2002; Ju et al, 2011; Staurengo-Ferrari et al, 2014a). To verify whether complex I would affect MSU crystals-triggered oxidative stress, 18 animals were randomly distributed in 3 groups of 6 animals.…”

Section: Resultsmentioning

confidence: 99%

“…Nitric oxide (NO) is a key molecule in pain modulation and its therapeutic effect in painful and inflammatory conditions has been demonstrated in different studies through the use of NO donors (Staurengo-Ferrari et al, 2013, 2014a). 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

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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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Quercetin inhibits gout arthritis in mice: induction of an opioid-dependent regulation of inflammasome

et al. 2017

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We investigated the anti-inflammatory and analgesic effects of quercetin in monosodium urate crystals (MSU)-induced gout arthritis, and the sensitivity of quercetin effects to naloxone, an opioid receptor antagonist. Mice were treated with quercetin, and mechanical hyperalgesia was assessed at 1-24 h after MSU injection. In vivo, leukocyte recruitment, cytokine levels, oxidative stress, NFκB activation, and gp91 and inflammasome components (NLRP3, ASC, Pro-caspase-1, and Pro-IL-1β) mRNA expression by qPCR were determined in the knee joints at 24 h after MSU injection. Inflammasome activation was determined, in vitro, in lipopolysaccharide-primed macrophages challenged with MSU. Quercetin inhibited MSU-induced mechanical hyperalgesia, leukocyte recruitment, TNFα and IL-1β production, superoxide anion production, inflammasome activation, decrease of antioxidants levels, NFκB activation, and inflammasome components mRNA expression. Naloxone pre-treatment prevented all the inhibitory effects of quercetin over MSU-induced gout arthritis. These results demonstrate that quercetin exerts analgesic and anti-inflammatory effect in the MSU-induced arthritis in a naloxone-sensitive manner.

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The ruthenium nitric oxide donor, [Ru(HEDTA)NO], inhibits acute nociception in mice by modulating oxidative stress, cytokine production and activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway

Cited by 11 publications

References 80 publications

Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-κB activation

Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-κB activation

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

Quercetin inhibits gout arthritis in mice: induction of an opioid-dependent regulation of inflammasome

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