Meloxicam ameliorates the cartilage and subchondral bone deterioration in monoiodoacetate-induced rat osteoarthritis

Nagy, E; Vajda, Enikő; Vari, Camil-Eugen; Sipka, Sándor; Fárr, Ana-Maria; Horváth, Emőke

doi:10.7717/peerj.3185

Cited by 24 publications

(25 citation statements)

References 45 publications

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“…Fourteen of the included studies have investigated chondroprotective actions of selective COX-2 inhibitors after systemic administration (Table 1). Most studies focused on chondroprotective actions of the selective COX-2 inhibitor celecoxib [12][13][14][15][16][17][18][19][20][21], while other studies investigated chondroprotective actions of meloxicam [22,23] and etoricoxib [24,25]. Four studies that investigated chondroprotective actions of selective COX-2 inhibitors in surgically induced OA models failed to demonstrate chondroprotective actions when the drug was administered directly after OA induction [12,14,18,22].…”

Section: Preclinical Studies: Oral and Intraperitoneal Administrationmentioning

confidence: 99%

“…In conclusion, there is conflicting evidence regarding the chondroprotective actions of systemically administered selective COX-2 inhibitors since five studies did not show chondroprotective actions, while nine studies showed chondroprotective actions after systemic administration with selective COX-2 inhibitors. Next to surgically induced OA models, the monosodium iodoacetate (MIA) rat OA model [16,17,23], the collagenase OA model [13,19] and the spontaneous OA mouse model (STR/Ort) [21] were also used to investigate chondroprotective actions of selective COX-2 inhibitors celecoxib [13,16,17,19,21] and meloxicam [23]. In these studies, chondroprotective actions of selective COX-2 inhibitors were observed after oral administration as evidenced by improved histological scores compared to the controls.…”

Section: Preclinical Studies: Oral and Intraperitoneal Administrationmentioning

confidence: 99%

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Chondroprotective Actions of Selective COX-2 Inhibitors In Vivo: A Systematic Review

Timur

Caron

Jeuken

et al. 2020

IJMS

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Knee osteoarthritis (OA) is a condition mainly characterized by cartilage degradation. Currently, no effective treatment exists to slow down the progression of OA-related cartilage damage. Selective COX-2 inhibitors may, next to their pain killing properties, act chondroprotective in vivo. To determine whether the route of administration is important for the efficacy of the chondroprotective properties of selective COX-2 inhibitors, a systematic review was performed according to the PRISMA guidelines. Studies investigating OA-related cartilage damage of selective COX-2 inhibitors in vivo were included. Nine of the fourteen preclinical studies demonstrated chondroprotective effects of selective COX-2 inhibitors using systemic administration. Five clinical studies were included and, although in general non-randomized, failed to demonstrate chondroprotective actions of oral selective COX-2 inhibitors. All of the four preclinical studies using bolus intra-articular injections demonstrated chondroprotective actions, while one of the three preclinical studies using a slow release system demonstrated chondroprotective actions. Despite the limited evidence in clinical studies that have used the oral administration route, there seems to be a preclinical basis for considering selective COX-2 inhibitors as disease modifying osteoarthritis drugs when used intra-articularly. Intra-articularly injected selective COX-2 inhibitors may hold the potential to provide chondroprotective effects in vivo in clinical studies.

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Section: Preclinical Studies: Oral and Intraperitoneal Administrationmentioning

confidence: 99%

Section: Preclinical Studies: Oral and Intraperitoneal Administrationmentioning

confidence: 99%

Chondroprotective Actions of Selective COX-2 Inhibitors In Vivo: A Systematic Review

Timur

Caron

Jeuken

et al. 2020

IJMS

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“…The use of meloxicam is increasing due to its high intrinsic activity. It is widely used in the treatment of osteoarthritis, rheumatoid arthritis and neurophatic pain in humans [6,7].…”

Section: Introductionmentioning

confidence: 99%

Abcg2 transporter affects plasma, milk and tissue levels of meloxicam

García-Lino

Blanco-Paniagua

Astorga-Simon

et al. 2020

Biochemical Pharmacology

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ATP-binding cassette (ABCG2) is an efflux transporter that extrudes xenotoxins from cells in liver, intestine, mammary gland, brain and other organs, affecting the pharmacokinetics, brain accumulation and secretion into milk of several compounds, including antitumoral, antimicrobial and anti-inflammatory drugs. The aim of this study was to investigate whether the widely used anti-inflammatory drug meloxicam is an Abcg2 sustrate, and how this transporter affects its systemic distribution. Using polarized ABCG2-transduced cell lines, we found that meloxicam is efficiently transported by murine Abcg2 and human ABCG2. After oral administration of meloxicam, the area under the plasma concentration-time curve in Abcg2-/mice was 2-fold higher than in wild type mice (146.06 ± 10.57 µg•h/ml versus 73.80 ± 10.00 µg•h/ml). Differences in meloxicam distribution were reported for several tissues, with a 20-fold higher concentration in the brain of Abcg2-/compared to wild-type mice. Meloxicam secretion into milk was also affected by the transporter, with a 2.5-fold higher milk-to-plasma ratio in wild-type compared with Abcg2-/lactating female mice (0.58 ± 0.08 versus 0.23 ± 0.06). We conclude that Abcg2 is an important determinant of the plasma and brain distribution of meloxicam and is clearly involved in its secretion into milk.

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“…They concluded that the drug could selectively modulate the expression of the glutamatergic signaling system components along the NMDA: AMPA receptor stoichiometry and repress glutamate excitotoxicity, leading to neuronal death. Meloxicam represses low-grade inflammation, even in non-vascularized tissues (126), and has a dual beneficial effect on extracellular matrix repair. Through its anti-fibrotic effect, downregulates the hydroxyproline production and collagen deposition, and it is angiostatic and anti-oxidant through stimulation of glutathione peroxidase, catalase, superoxide dismutase, and decrease of lipid peroxidation and myeloperoxidase activity (127,128).…”

Section: Experimental Evidence For Pharmacological Checkpoints Of Infmentioning

confidence: 99%

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

et al. 2020

Self Cite

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Increasing evidence hints to the central role of neuroinflammation in the development of post-stroke depression. Danger signals released in the acute phase of ischemia trigger microglial activation, along with the infiltration of neutrophils and macrophages. The increased secretion of proinflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor α (TNFα) provokes neuronal degeneration and apoptosis, whereas IL-6, interferon γ (IFNγ), and TNFα induce aberrant tryptophane degradation with the accumulation of the end-product quinolinic acid in resident glial cells. This promotes glutamate excitotoxicity via hyperexcitation of N-methyl-D-aspartate receptors and antagonizes 5-hydroxy-tryptamine, reducing synaptic plasticity and neuronal survival, thus favoring depression. In the post-stroke period, CX3CL1 and the CD200-CD200R interaction mediates the activation of glial cells, whereas CCL-2 attracts infiltrating macrophages. CD206 positive cells grant the removal of excessive danger signals; the high number of regulatory T cells, IL-4, IL-10, transforming growth factor β (TGFβ), and intracellular signaling via cAMP response element-binding protein (CREB) support the M2 type differentiation. In favorable conditions, these cells may exert efficient clearance, mediate tissue repair, and might be essential players in the downregulation of molecular pathways that promote post-stroke depression. Contents 1. Introduction: Systemic and neuroinflammation are both characteristic in certain forms of post-stroke depression 2. Post-stroke depression, genetic factors and lesion localization 3. Brain-derived neurotrophic factor: A link between purinergic signaling, neuroinflammation and depression 4. The post-stroke immune pathways and tissue repair 5. The microglia/macrophage network in post-stroke depression 6. Mediators of neuroinflammation are key elements in the post-ischemic response 7. Experimental evidence for pharmacological checkpoints of inflammation 8. Discussion 1. Introduction: Systemic and neuroinflammation are both characteristic in certain forms of post-stroke depression Stroke is a medical emergency that frequently results in severe neurological sequelae and other complex dysfunctions. Among these, post-stroke depression (PSD) is prevalent, being

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Meloxicam ameliorates the cartilage and subchondral bone deterioration in monoiodoacetate-induced rat osteoarthritis

Cited by 24 publications

References 45 publications

Chondroprotective Actions of Selective COX-2 Inhibitors In Vivo: A Systematic Review

Chondroprotective Actions of Selective COX-2 Inhibitors In Vivo: A Systematic Review

Abcg2 transporter affects plasma, milk and tissue levels of meloxicam

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

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