Buprenorphine Alters Inflammatory and Oxidative Stress Molecular Markers in Arthritis

Hemshekhar, Mahadevappa; Anaparti, Vidyanand; Hitchon, Carol; Mookherjee, Neeloffer

doi:10.1155/2017/2515408

Cited by 23 publications

(40 citation statements)

References 23 publications

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“…In addition, methadone seems to have a more severe effect as indicated by the significantly lower values of catalase compared to buprenorphine. These results are supported by previous findings [49–52]. Specifically, methadone appears to have a greater impact on lowering antioxidant defence since patients under MMT have shown a depletion of GSH and CAT levels [50, 52].…”

Section: Discussionsupporting

confidence: 90%

Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

Leventelis

Goutzourelas

Kortsinidou

et al. 2019

Oxidative Medicine and Cellular Longevity

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Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n=21) and the methadone (n=21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n=29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.

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Section: Discussionsupporting

confidence: 90%

Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

Leventelis

Goutzourelas

Kortsinidou

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…The protocol used for the CIA murine model was based on our previous study [ 30 ] and approved by The University of Manitoba Animal Research Ethics Board. Experimental design and reporting of data is compliant with the ARRIVE guidelines for in vivo animal research [ 34 ].…”

Section: Methodsmentioning

confidence: 99%

A bioavailable form of curcumin, in combination with vitamin-D- and omega-3-enriched diet, modifies disease onset and outcomes in a murine model of collagen-induced arthritis

et al. 2021

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Objective Curcumin (CUR), vitamin D3 (D3), and omega-3-fatty acids (O3FA) individually modulate inflammation and pain in arthritis. Although these supplements are widely used, their combinatorial effects have not been defined. In this study, we examined the effects of a D3 and O3FA (VO)-enriched diet in conjunction with a highly bioavailable form of CUR (Cureit/Acumin™) in a collagen-induced arthritis (CIA) murine model. Methods Male DBA/1J mice were acclimatized to VO-enriched diet and challenged with bovine collagen II (CII). Bioavailable CUR was administered daily by oral gavage from the onset of CII challenge. Disease severity was determined by monitoring joint thickness and standardized clinical score. Cellular infiltration and cartilage degradation in the joints were assessed by histology, serum cytokines profiled by Meso Scale Discovery multiplex assay, and joint matrix metalloproteinases examined by western blots. Results CUR by itself significantly decreased disease severity by ~ 60%. Administration of CUR in CIA mice taking a VO-enriched diet decreased disease severity by > 80% and maximally delayed disease onset and progression. Some of the disease-modifying effects was mediated by CUR alone, e.g., suppression of serum anti-collagen antibodies and decrease of cellular infiltration and MMP abundance in the joints of CIA mice. Although CUR alone suppressed inflammatory cytokines in serum of CIA mice, the combination of CUR and VO diet significantly enhanced the suppression (> 2-fold compared to CUR) of TNF, IFN-γ, and MCP-1, all known to be associated with RA pathogenesis. Conclusion This study provides proof-of-concept that the combination of bioavailable CUR, vitamin D3, and O3FA substantially delays the development and severity of CIA. These findings provide a rationale for systematically evaluating these widely available supplements in individuals at risk for developing future RA.

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“…These synthetic peptides were resuspended in sterile saline and administered by s.c. injections (6 mg/kg body weight) in both models. The dose and mode of administration of these peptides were based on our previous studies in the CIA model and HDM-challenge model (24)(25)(26)(27). In the CIA model, the peptides were administered starting from day 20 [1 day before boost, after the initial arthritis induction phase (32)] and subsequently every 48 h until the end of the study.…”

Section: Administration Of Cathelicidin-derived Synthetic Peptides Inmentioning

confidence: 99%

“…In this study, we investigated the abundance of the mouse cathelicidin CRAMP, α -and β-defensins, and calprotectin subunits S100A8 and S100A9, in the two different murine models of chronic inflammation; a CIA model of inflammatory arthritis and allergen HDM-challenged model of airway inflammation (25)(26)(27). We showed that CRAMP and calprotectin subunits S100A8, and S100A9 are disparately altered in these mouse models, being significantly increased in the joint tissues of CIA mice, but decreased in the HDM-challenged lungs.…”

Section: Introductionmentioning

confidence: 99%

Cathelicidin and Calprotectin Are Disparately Altered in Murine Models of Inflammatory Arthritis and Airway Inflammation

et al. 2020

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Cationic host defense peptides (CHDP) are immunomodulatory molecules that control infections and contribute to immune homeostasis. CHDP such as cathelicidin and calprotectin expression is altered in the arthritic synovium, and in the lungs of asthma and COPD patients. Recent studies suggest a link between airway inflammation and the immunopathology of arthritis. Therefore, in this study we compared the abundance of mouse cathelicidin (CRAMP), defensins, and calprotectin subunits (S100A8 and S100A9) in murine models of collagen-induced arthritis (CIA) and allergen house dust mite (HDM)-challenged airway inflammation. CRAMP, S100A8, and S100A9 abundance were significantly elevated in the joint tissues of CIA mice, whereas these were decreased in the lung tissues of HDM-challenged mice, compared to naïve. We further compared the effects of administration of two different synthetic immunomodulatory peptides, IG-19 and IDR-1002, on cathelicidin and calprotectin abundance in the two models. Administration of IG-19, which controls disease progression and inflammation in CIA mice, significantly decreased CRAMP, S100A8, and S100A9 levels to baseline in the joints of the CIA mice, which correlated with the decrease in cellular influx in the joints. However, administration of IDR-1002, which suppresses HDM-induced airway inflammation, did not prevent the decrease in the levels of cathelicidin and calprotectin in the lungs of HDM-challenged mice. Cathelicidin and calprotectin levels did not correlate with leukocyte accumulation in the lungs of the HDM-challenged mice. Results of this study suggest that endogenous cathelicidin and calprotectin abundance are disparately altered, and may be differentially regulated, within local tissues in airway inflammation compared to arthritis.

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Buprenorphine Alters Inflammatory and Oxidative Stress Molecular Markers in Arthritis

Cited by 23 publications

References 23 publications

Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

A bioavailable form of curcumin, in combination with vitamin-D- and omega-3-enriched diet, modifies disease onset and outcomes in a murine model of collagen-induced arthritis

Cathelicidin and Calprotectin Are Disparately Altered in Murine Models of Inflammatory Arthritis and Airway Inflammation

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