Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis

Ferrándiz, Marı́a Luisa; Maicas, Nuria; García-Arnandis, Isabel; Terencio, María Carmen; Motterlini, Roberto; Devesa, Isabel; Joosten, Leo A. B.; Berg, Wim B. van den; Alcaraz, Marı́a José

doi:10.1136/ard.2007.082412

Cited by 82 publications

(57 citation statements)

References 33 publications

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“…Indeed, the administration of carbon monoxide-releasing molecules-a new class of chemical agents able to reproduce several biologic effects of HO-1-derived carbon monoxide, or the HO-1 inducer compound, cobalt protoporphyrin IX (CoPP)-inhibits inflammation, acute nociception, and neuropathic pain (Ferrándiz et al, 2008;Rosa et al, 2008;Egea et al, 2009;Maicas et al, 2010;Hervera et al, 2013a;Negrete et al, 2014). We have also recently demonstrated that carbon monoxide synthesized by HO-1 modulates the effects of morphine but not of DPDPE and JWH-015 under neuropathic pain conditions (Hervera et al, 2013b), although the role played by CoPP treatment on the effects and expression of MOR, DOR, and CB2R during chronic inflammatory pain has not been evaluated.…”

Section: Introductionmentioning

confidence: 99%

Treatment with a Heme Oxygenase 1 Inducer Enhances the Antinociceptive Effects of µ-Opioid, δ-Opioid, and Cannabinoid 2 Receptors during Inflammatory Pain

Carcolé

Castany

Leánez

et al. 2014

J Pharmacol Exp Ther

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The administration of m-opioid receptor (MOR), d-opioid receptor (DOR), and cannabinoid 2 receptor (CB2R) agonists attenuates inflammatory pain. We investigated whether treatment with the heme oxygenase 1 (HO-1) inducer, cobalt protoporphyrin IX (CoPP), could modulate the local effects and expression of MOR, DOR, or CB2R during chronic inflammatory pain. In mice with inflammatory pain induced by the subplantar administration of complete Freund's adjuvant, we evaluated the effects of the intraperitoneal administration of 10 mg/kg CoPP on the antiallodynic and antihyperalgesic actions of locally administeredagonists and its reversion with the HO-1 inhibitor, tin protoporphyrin IX (SnPP). The effect of CoPP treatment on the dorsal root ganglia expression of HO-1, MOR, DOR, and CB2R was also assessed. The results show that treatment with CoPP increased the local antinociceptive effects produced by morphine, DPDPE, or JWH-015 during chronic inflammatory pain, and these effects were blocked by the subplantar administration of SnPP, indicating the participation of HO-1 in the antinociceptive actions. CoPP treatment, apart from inducing the expression of HO-1, also enhanced the expression of MOR, did not alter CB2R, and avoided the decreased expression of DOR induced by inflammatory pain. This study shows that the HO-1 inducer (CoPP) increased the local antinociceptive effects of MOR, DOR, and CB2R agonists during inflammatory pain by altering the peripheral expression of MOR and DOR. Therefore, the coadministration of CoPP with local morphine, DPDPE, or JWH-015 may be a good strategy for the management of chronic inflammatory pain.

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Section: Introductionmentioning

confidence: 99%

Treatment with a Heme Oxygenase 1 Inducer Enhances the Antinociceptive Effects of µ-Opioid, δ-Opioid, and Cannabinoid 2 Receptors during Inflammatory Pain

Carcolé

Castany

Leánez

et al. 2014

J Pharmacol Exp Ther

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“…The protective effects of CO for autoimmune diseases have also been reported [32]. In a murine collagen-induced arthritis model, CORM reduced inflammation, RANKL expression and joint destruction [16]. Furthermore, in RANKL-stimulated RAW 246.7 cells, we previously showed that CO suppressed osteoclastogenesis [23].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, carbon monoxide (CO) inhibits RANKL signaling and therefore osteoclastogenesis, resulting in decreased bone loss associated with ovariectomy in mice [13], and treatment with CO releasing molecule-2 (CORM-2) inhibited RANKL-induced osteoclastogenesis in primary cultures of osteoclast precursors in a dose-dependent manner [14]. In a murine collageninduced arthritis model, CO reduced inflammation and decreased the number of osteoclasts [15], and CORM reduced RANKL expression and joint destruction [16]. However, the mechanisms by which CO elicit these effects remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Carbon Monoxide Inhibits Receptor Activator of NF-κB (RANKL)-Induced Osteoclastogenesis

Tseng

Chia

Wang

et al. 2015

Cell Physiol Biochem

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Background: Low concentrations of carbon monoxide (CO) have anti-inflammatory effects and can reduce bone erosion in a murine collagen-induced arthritis model. The objective of this study was to assess the effects of CO on receptor activator of NF-γB ligand (RANKL), one of the key stimulators of osteoclastogenesis. Methods: The in vivo effects of CO on RANKL expression were assessed in a collagen antibody-induced arthritis model in mice. Cell proliferation and apoptosis were assessed in the RAW246.7 cell line stimulated with RANKL and exposed to either air or CO. The number of tartrate resistant acid phosphatase (TRAP)-positive RAW246.7 cells was also examined after treatment with RANKL and the peroxisome proliferator-activated receptor gamma (PPARγ) agonist, Troglitazone. Results: CO reduced RANKL expression in the synovium of arthritic mice. Although CO slightly increased RAW246.7 cell proliferation, no differences in activated caspase 3 levels were detected. In addition, Troglitazone ameliorated the inhibitory effects of CO on RANKL-induced TRAP expression by RAW246.7 cells. Conclusions: CO suppresses osteoclast differentiation by inhibiting the RANKL-induced activation of PPAR-γ. Given the role of the PPAR-γ/cFos (AP-1) pathway in regulating the transcription factor, NFATc1, the master regulator of osteoclastogenesis, further studies are warranted to explore CO in treating inflammatory bone disorders.

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“…Local inflammation of the joints is a key link in the process of its pathogenesis; bone loss or damage caused by inflammation is the result of changes to the joints in RA, and symptoms of pain associated with joint swelling are often the most severe symptoms of which the patient complains (9). Therefore, inhibiting the inflammation has become one of the predominant targets of the clinical treatment (16). In the present study, the administration of polydatin (30 or 45 mg/kg) markedly ameliorated reactive inflammation in CIA mice.…”

Section: Discussionmentioning

confidence: 99%

“…RA is a type of chronic, systemic autoimmune disease which has the predominant feature of symmetrical polyarthritis, and anti-inflammatory analgesic symptomatic treatments, which would delay the development of the disease, offer the major therapeutic options (2,16). Local inflammation of the joints is a key link in the process of its pathogenesis; bone loss or damage caused by inflammation is the result of changes to the joints in RA, and symptoms of pain associated with joint swelling are often the most severe symptoms of which the patient complains (9).…”

Section: Discussionmentioning

confidence: 99%

Effective treatment of polydatin weakens the symptoms of collagen-induced arthritis in mice through its anti-oxidative and anti-inflammatory effects and the activation of MMP-9

Wang

2016

Molecular Medicine Reports

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Abstract. Polydatin is a natural extract used in traditional Chinese medicine, which leads to a marked improvement in the microcirculation perfusion and enhances the animal myocardial contraction force. The present study aimed to determine whether an effective treatment of polydatin ameliorates the symptoms of collagen-induced arthritis (CIA), and also to explore the potential mechanism. Male DBA/1J mice were induced into CIA model mice. The administration of polydatin effectively suppressed CIA in mice. The serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) were effectively increased following the induction of CIA in the model mice compared with the control group. The elevated serum levels of MDA, SOD, TNF-α and IL-1β were markedly suppressed by the effective treatment of polydatin in CIA mice, compared with the CIA model group. However, an increase in the level of matrix metalloproteinase-9 (MMP-9) was markedly induced in the CIA mice compared with the control group. As compared with the CIA group, the expression of MMP-9 was substantially reduced by the effective treatment of polydatin. Taken together, the effective treatment of polydatin ameliorated the symptoms of CIA through an exertion of its antioxidative and anti-inflammatory effects, and also via activation of the expression of matrix metalloproteinase-9 (MMP-9) in mice.

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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis

Abstract: This study reveals the antiarthritic properties of CORM-3 in the CIA model and supports the notion that CO-RMs could be developed as a novel strategy for the treatment of inflammatory and arthritic conditions.

Cited by 82 publications

References 33 publications

Treatment with a Heme Oxygenase 1 Inducer Enhances the Antinociceptive Effects of µ-Opioid, δ-Opioid, and Cannabinoid 2 Receptors during Inflammatory Pain

Treatment with a Heme Oxygenase 1 Inducer Enhances the Antinociceptive Effects of µ-Opioid, δ-Opioid, and Cannabinoid 2 Receptors during Inflammatory Pain

Carbon Monoxide Inhibits Receptor Activator of NF-κB (RANKL)-Induced Osteoclastogenesis

Effective treatment of polydatin weakens the symptoms of collagen-induced arthritis in mice through its anti-oxidative and anti-inflammatory effects and the activation of MMP-9

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