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6 results on '"CORM-2"'

1. CORM-2 Pretreatment Attenuates Inflammation-mediated Islet Dysfunction.

Author

Cai XH, Wang GQ, Liang R, Wang L, Liu TL, Zou JQ, Liu N, Liu Y, Wang SS, and Shen ZY

Subjects
Animals, Anti-Inflammatory Agents therapeutic use, Flow Cytometry, Glucose Tolerance Test, Humans, Immunohistochemistry, Inflammation metabolism, Intercellular Adhesion Molecule-1 metabolism, Interleukin-1beta metabolism, Interleukin-6 metabolism, Islets of Langerhans Transplantation, Male, Mice, Inbred BALB C, Toll-Like Receptor 4 metabolism, Tumor Necrosis Factor-alpha metabolism, Inflammation drug therapy, Organometallic Compounds therapeutic use
Abstract

During the process of human islet isolation a cascade of stressful events are triggered and negatively influence islet yield, viability, and function, including the production of proinflammatory cytokines and activation of apoptosis. Carbon monoxide-releasing molecule 2 (CORM-2) is a donor of carbon monoxide (CO) and can release CO spontaneously. Accumulating studies suggest that CORM-2 exerts cytoprotective and anti-inflammatory properties. However, the effect of CORM-2 on islet isolation is still unclear. In this study, we found that CORM-2 pretreatment significantly decreased the expression of critical inflammatory genes, including tissue factor , intercellular adhesion molecule-1 , chemokine ( C-C motif ) ligand 2 , C-X-C motif chemokine 10 , Toll-like receptor 4 , interleukin-1β , interleukin-6 , and tumor necrosis factor-α ( TNF-α ). The isolated islets of the CORM-2 pretreatment group showed reduced apoptotic rate, improved viability, and higher glucose-stimulated insulin secretion, and functional gene expression in comparison to control group. Importantly, CORM-2 pretreatment prevented the impairment caused by TNF-α, evidenced by the improved glucose-stimulated index and transplantation outcomes. The present study demonstrated the anti-inflammatory property of CORM-2 during human islet isolation, and we suggest that CORM-2 pretreatment is an appealing treatment to mitigate inflammation-mediated islet dysfunction during isolation and culture ex vivo and to preserve long-term islet survival and function.

Published
2020
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2. CORM-2-entrapped ultradeformable liposomes ameliorate acute skin inflammation in an ear edema model via effective CO delivery

Author

Alam Zeb, Yeong-Hwan Choe, Omer Salman Qureshi, Young-Jun Shin, Inbo Han, Donghyun Kim, Sun-Young Chang, Kyoung-Won Kim, Eun-Hye Kim, Gwan-Yeong Lee, Jin-Ki Kim, Ok-Nam Bae, Ho-Ik Choi, Beomseon Suh, and Cheol Ho Lee

Subjects
medicine.medical_treatment, Inflammation, Pharmacology, Proinflammatory cytokine, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Phosphatidylcholine, medicine, General Pharmacology, Toxicology and Pharmaceutics, Nitrite, Lipid bilayer, Carbon monoxide, Ultradeformable liposomes, 030304 developmental biology, 0303 health sciences, Liposome, Chemistry, Activator (genetics), Anti-inflammatory effect, lcsh:RM1-950, Skin inflammation, Ear edema, Cytokine, lcsh:Therapeutics. Pharmacology, 030220 oncology & carcinogenesis, Original Article, medicine.symptom, CORM-2
Abstract

The short release half-life of carbon monoxide (CO) is a major obstacle to the effective therapeutic use of carbon monoxide-releasing molecule-2 (CORM-2). The potential of CORM-2-entrapped ultradeformable liposomes (CORM-2-UDLs) to enhance the release half-life of CO and alleviate skin inflammation was investigated in the present study. CORM-2-UDLs were prepared by using soy phosphatidylcholine to form lipid bilayers and Tween 80 as an edge activator. The deformability of CORM-2-UDLs was measured and compared with that of conventional liposomes by passing formulations through a filter device at a constant pressure. The release profile of CO from CORM-2-UDLs was evaluated by myoglobin assay. In vitro and in vivo anti-inflammatory effects of CORM-2-UDLs were assessed in lipopolysaccharide-stimulated macrophages and TPA-induced ear edema model, respectively. The deformability of the optimized CORM-2-UDLs was 2.3 times higher than conventional liposomes. CORM-2-UDLs significantly prolonged the release half-life of CO from 30 s in a CORM-2 solution to 21.6 min. CORM-2-UDLs demonstrated in vitro anti-inflammatory activity by decreasing nitrite production and pro-inflammatory cytokine levels. Furthermore, CORM-2-UDLs successfully ameliorated skin inflammation by reducing ear edema, pathological scores, neutrophil accumulation, and inflammatory cytokines expression. The results demonstrate that CORM-2-UDLs could be used as promising therapeutics against acute skin inflammation., Graphical abstract The short release half-life of carbon monoxide is a major obstacle to the effective therapeutic use of carbon monoxide-releasing molecule-2 (CORM-2). Herein, CORM-2-entrapped ultradeformable liposomes (CORM-2-UDLs) were designed to prolong carbon monoxide release half-life and enhance skin permeation of CORM-2 for better anti-inflammatory effects in skin inflammation model.Image 1

Published
2020

3. CORM-2 Pretreatment Attenuates Inflammation-mediated Islet Dysfunction

Author

Zhongyang Shen, Jia-Qi Zou, Yan Liu, Xiang-Heng Cai, Teng-Li Liu, Le Wang, Guan-Qiao Wang, Na Liu, Shusen Wang, and Rui Liang

Subjects
Male, Chemokine, Interleukin-1beta, islet function, Biomedical Engineering, Anti-Inflammatory Agents, Islets of Langerhans Transplantation, lcsh:Medicine, Inflammation, Pharmacology, Proinflammatory cytokine, Tissue factor, medicine, Organometallic Compounds, Animals, Humans, Receptor, Transplantation, geography, Mice, Inbred BALB C, geography.geographical_feature_category, biology, Chemistry, Interleukin-6, Tumor Necrosis Factor-alpha, islet transplantation, lcsh:R, Cell Biology, Glucose Tolerance Test, Islet, Flow Cytometry, Intercellular Adhesion Molecule-1, Immunohistochemistry, Toll-Like Receptor 4, TNF-α, biology.protein, Tumor necrosis factor alpha, Original Article, medicine.symptom, Ex vivo, CORM-2
Abstract

During the process of human islet isolation a cascade of stressful events are triggered and negatively influence islet yield, viability, and function, including the production of proinflammatory cytokines and activation of apoptosis. Carbon monoxide-releasing molecule 2 (CORM-2) is a donor of carbon monoxide (CO) and can release CO spontaneously. Accumulating studies suggest that CORM-2 exerts cytoprotective and anti-inflammatory properties. However, the effect of CORM-2 on islet isolation is still unclear. In this study, we found that CORM-2 pretreatment significantly decreased the expression of critical inflammatory genes, including tissue factor, intercellular adhesion molecule-1, chemokine ( C-C motif) ligand 2, C-X-C motif chemokine 10, Toll-like receptor 4, interleukin-1β, interleukin-6, and tumor necrosis factor-α ( TNF-α). The isolated islets of the CORM-2 pretreatment group showed reduced apoptotic rate, improved viability, and higher glucose-stimulated insulin secretion, and functional gene expression in comparison to control group. Importantly, CORM-2 pretreatment prevented the impairment caused by TNF-α, evidenced by the improved glucose-stimulated index and transplantation outcomes. The present study demonstrated the anti-inflammatory property of CORM-2 during human islet isolation, and we suggest that CORM-2 pretreatment is an appealing treatment to mitigate inflammation-mediated islet dysfunction during isolation and culture ex vivo and to preserve long-term islet survival and function.

Published
2020

4. Effect of Carbon Monoxide Donor CORM-2 on Vitamin D3 Metabolism.

Author

Feger, Martina, Fajol, abul, Lebedeva, aleksandra, Meissner, adrian, Michael, Diana, Voelkl, Jakob, alesutan, Ioana, Schleicher, Erwin, Reichetzeder, Christoph, Hocher, Berthold, Qadri, Syed M., and Lang, Florian

Subjects
*CARBON monoxide, *VITAMIN D metabolism, *INFLAMMATION, *ENZYMES, *PHOSPHATE transport proteins, *WESTERN immunoblotting
Abstract

Background/Aims: Carbon monoxide (CO) interferes with cytochrome-dependent cellular functions and acts as gaseous transmitter. CO is released from CO-releasing molecules (CORM) including tricarbonyl-dichlororuthenium (II) dimer (CORM-2), molecules considered for the treatment of several disorders including vascular dysfunction, inflammation, tissue ischemia and organ rejection. Cytochrome P450-sensitive function include formation of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) by renal 25-hydroxyvitamin D3 1-alpha-hydroxylase (Cyp27b1). The enzyme is regulated by PTH, FGF23 and klotho. 1,25(OH)2D3 regulates Ca2+ and phosphate transport as well as klotho expression. The present study explored, whether CORM-2 influences 1,25(OH)2D3 formation and klotho expression. Methods: Mice were treated with intravenous CORM-2 (20 mg/kg body weight). Plasma 1,25(OH)2D3 and FGF23 concentrations were determined by ELISA, phosphate, calcium and creatinine concentrations by colorimetric methods, transcript levels by quantitative RT-PCR and protein expression by western blotting. Fgf23 mRNA transcript levels were further determined in rat osteosarcoma UMR106 cells without or with prior treatment for 24 hours with 20 µM CORM-2. Results: CORM-2 injection within 24 hours significantly increased FGF23 plasma levels and decreased 1,25(OH)2D3 plasma levels, renal Cyp27b1 gene expression as well as renal klotho protein abundance and transcript levels. Moreover, treatment of UMR106 cells with CORM-2 significantly increased Fgf23 transcript levels. Conclusion: CO-releasing molecule CORM-2 enhances FGF23 expression and release and decreases klotho expression and 1,25(OH)2D3 synthesis. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2013
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5. Activation of PPAR-γ by Carbon Monoxide from CORM-2 Leads to the Inhibition of iNOS but not COX-2 Expression in LPS-Stimulated Macrophages.

Author

Tsoyi, Konstantin, Ha, Yu, Kim, Young, Lee, Young, Kim, Hyo, Kim, Hye, Seo, Han, Lee, Jae, and Chang, Ki

Subjects
*CARBON monoxide, *MACROPHAGES, *NITRIC oxide, *CYCLOOXYGENASE 2, *HEME oxygenase, *THERAPEUTICS
Abstract

The effect of CO on the expression of iNOS and COX-2 was investigated by using a CO-releasing molecule (CORM)-2 in LPS-activated RAW 264.7 cells in vitro. Interestingly, CORM-2 significantly inhibited iNOS (NO) but not COX-2 (PGE2) expression. PPAR-γ activators such as troglitazone, GW1929, and 15-deoxy-Δ12, 14- prostaglandin J2 showed preferential inhibitory effect on iNOS over COX-2 expression in LPS-activated macrophages. The same effect was shown in lung tissues (iNOS, COX-2) and serum (NO, PGE2) when administered of CORM-2 in LPS-induced septic mice, indicating that CO derived from CORM-2 differentially regulates iNOS and COX-2 through PPAR-γ activation under inflammation state. [ABSTRACT FROM AUTHOR]

Published
2009
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6. The role of iron in inflammatory oligodendrocyte pathology: From clinical to cell culture

Author

Johnson, Erika B

Subjects
Microglia, SnPP, Inflammation, TR33B, Iron, Hemin, CORM-2, Co-culture, MRI, Multiple sclerosis
Abstract

Abstract: MS is a chronic demyelinating disease of the CNS that presents with debilitating symptoms in the later stages of disease progression and therefore a high demand for targeted disease-modifying treatments exists. In order to create effective treatments the causalities between the symptoms and pathological mechanisms of the disease need to be properly understood. One such area that remains poorly understood is the role of excess iron deposition in disease aetiology and progression. Literature has shown excess iron deposition in the brains of those with MS. However, whether it is the concentration of excess deposition, the brain-specific regions of deposition, or even the method of iron deposition/metabolism that causes this excess deposition is not understood. This thesis presents a set of experiments that observe the possible role of iron on inflammatory oligodendrocyte pathology, from a macro-to a micro-level. First, the deposition pattern of iron in regards to gross anatomy in brains affected by MS is observed and quantified using MRI images as well as tissue samples. The data presented here suggests that both the severity and/or maturity of the lesion play a role in the level of excess and pattern of iron deposition. Second, a set of experiments are performed that manipulate a pathway crucial to iron homeostasis as well as a group of receptors implicated in the disease progression of MS (HO-1 and P2X respectively) to elucidate possible synergistic activity between them. The results suggest an association between the purinergic receptors and the HO-1 pathway.

Published
2017

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