Adjuvant arthritis as a model of inflammatory cachexia

Roubenoff, Ronenn; Freeman, Lisa M.; Smith, Donald E.; Abad, Leslie W.; Dinarello, Charles A.; Kehayias, Joseph J.

doi:10.1002/art.1780400320

Cited by 149 publications

(106 citation statements)

References 10 publications

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“…This result contrasts with that obtained in the present study, since administration of PEG-sTNFRI to arthritic rats stimulates food intake but does not alter gastrocnemius weight. These results support previous observations (Roubenoff et al 1997) which demonstrate that although adjuvant arthritis decreases food intake, cachexia is not the result of the decrease in caloric intake. PEG-sTNFRI administration did not change gastrocnemius weight in control or in arthritic rats.…”

Section: Discussionsupporting

confidence: 92%

“…Adjuvant-induced arthritis is an animal model for chronic inflammation and rheumatoid arthritis characterized by a decrease in body weight and cachexia (Roubenoff et al 1997, Ibáñez de Cáceres et al 2000. Cachexia, which also prevails in other situations such as burns, sepsis and cancer, is characterized by anorexia and tissue wasting, reflected essentially in a loss of adipose tissue and skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

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Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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Chronic inflammation is associated with a decrease in body weight and cachexia, which is characterized by anorexia and skeletal muscle wasting. The expression of atrogens muscle RING finger-1 (MuRF-1) and muscle atrophy F-box (MAFbx) are increased in muscle atrophy and it is known that tumour necrosis factor (TNF) regulates skeletal muscle loss through TNF receptor p55 (TNFRI). The aim of this study was to examine the effect of polyethylene glycol linked to soluble TNFRI (PEG-sTNFRI) on gene expression of the atrogens MuRF-1 and MAFbx in skeletal muscle of arthritic rats. Rats were injected with Freund's adjuvant and, 15 days later, arthritic and control rats were injected daily with PEG-sTNFRI (1 mg/kg, s.c.) or saline for 8 days. Arthritis decreased body weight gain, the weight of skeletal muscle and adipose mass. PEG-sTNFRI administration increased body weight gain and adipose mass of arthritic rats; however, it did not modify the skeletal muscle weight. The gene expression of TNF-a, MuRF1 and MAFbx, IGF-I and IGFBP-5 were increased in the skeletal muscle of arthritic rats, and the administration of PEG-sTNFRI did not modify these parameters. These data suggest that the anti-TNF agent PEG-sTNFRI did not prevent the increase in E3 ubiquitinligating enzymes, MuRF1 and MAFbx, gene expression in the skeletal muscle of arthritic rats.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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“…Similarly, rheumatoid cachexia is thought to be the outcome of cytokine mediated hypermetabolism (Roubenoff et al, 1997). Earlier reports have also recommended that absorption of 14 C-glucose and 14 Cleucine in rat's intestine become reduced during inflammatory condition (Somasundaran et al, 1983a) and anti-inflammatory drugs rectify the impaired absorption capacity of intestine (Somasundaran et al, 1983b).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of in vitro and in vivo anti-arthritic potential of Berberis calliobotrys

Alamgeer

Hasan

Uttra

et al. 2015

Bangladesh J Pharmacol

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The present study was commenced to evaluate the anti-arthritic effect of 70% methanol extract and n-butanol and aqueous fractions of Berberis calliobotrys using both in vitro and in vivo arthritis models. Extract and fractions were investigated in vitro for inhibition of protein (bovine serum and egg albumin) denaturation and human red blood cell membrane stabilization. In vivo anti-arthritic activity of extract and fractions at 50, 100 and 200 mg/kg was assessed using turpentine oil and formaldehyde-induced arthritis, while, 200 mg/kg dose was evaluated against complete Freund’s adjuvant-induced arthritis. B. calliobotrys produced significant (p<0.001) dose dependent inhibition of protein denaturation and human red blood cell membrane stabilization. In turpentine oil, formaldehyde and complete Freund’s adjuvant-induced arthritis models, B. calliobotrys significantly (p<0.001) reduced joint and paw swelling. B. calliobotrys markedly improved body weight, hematology profile, radiological and histopathological parameters in complete Freund’s adjuvant model. It could be concluded that B. calliobotrys holds anti-arthritic potential, supporting its traditional use in treatment of rheumatoid arthritis.

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“…For example, in rheumatoid arthritis, there is a dramatic increase in circulating proinflammatory cytokines. Furthermore, under these conditions membrane lipids are altered, and there is a severe impairment of energy homeostasis due to mitochondrial dysfunction of an unclear etiology (Ishizuki and Fujihira, 1984;Yamaguchi et al, 1989;Roubenoff et al, 1997).…”

Section: Proinflammatory Conditionsmentioning

confidence: 99%

Animal Models of Human Disease in Drug Safety Assessment

Boelsterli

2003

J. Toxicol. Sci.

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-Animal models of human disease have been widely used in drug discovery, but they are rarely utilized in toxicological research and screening (except for transgenic models in carcinogenicity testing). Although genetic and/or acquired pathophysiological alterations associated with a particular disease may greatly exacerbate toxic responses to drugs in certain patient subsets, these pre-existing pathological conditions are usually not considered in preclinical safety assessment. Examples of disease-related determinants of susceptibility include disruption of the cytokine network in pro-inflammatory conditions, mitochondrial alterations and oxidative stress in certain neurodegenerative diseases, altered antioxidant defense in certain viral infections, and altered gene expression and mitochondrial dysfunction in type 2 diabetes. Hence, if cellular stress caused by drugs or metabolites and the disease-related effects are superimposed, then an individual can become sensitized to potential drug toxicity. Animal models of modest inflammation indeed can potentiate the toxicity of certain drugs. Similarly, rodent models of type 2 diabetes predispose the animals to hepatotoxic effects of thiazolidinediones antidiabetics. In conclusion, it is suggested that tailor-made and simplified models be adopted and increasingly used, in spite of clear limitations, as optimal substrates for satellite toxicity studies to facilitate candidate selection, help predict rare and unexpected toxicity, and identify new biomarkers.

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Adjuvant arthritis as a model of inflammatory cachexia

Cited by 149 publications

References 10 publications

Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

Evaluation of <i>in vitro</i> and <i>in vivo</i> anti-arthritic potential of <i>Berberis calliobotrys</i>

Animal Models of Human Disease in Drug Safety Assessment

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