Morphological changes in hind limb muscles elicited by adjuvant‐induced arthritis of the rat knee

Ozawa, Junya; Kurose, Tomoyuki; Kawamata, Seiichi; Yamaoka, Kaoru

doi:10.1111/j.1600-0838.2009.00900.x

Cited by 13 publications

(16 citation statements)

References 35 publications

(46 reference statements)

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“…In arthritis, WBCs are elevated due to amplification of the IL-1β level. We have also observed increase in the level of ESR due to initiation of production of endogenous proteins (e.g., fibrinogen and α/β globulin), which also contributes to the progression of disease [21,22]. CFA-induced arthritic rats showed decreased levels of Hb due to destruction of premature RBCs and slow response of bone marrow erythropoietin.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Pinitol Against Inflammatory Mediators of Rheumatoid Arthritis via Inhibition of Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22)

et al. 2017

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BackgroundThe aim of the current study was to explore the anti-arthritic effect of pinitol via assessing its effect on various inflammatory mediators and its possible mechanism of action.Material/MethodWe assessed the anti-arthritic effect of pinitol in a formaldehyde- and CFA-induced arthritic model in Wistar Swiss albino strain rats divided into 6 groups. The rats received different doses of pinitol and indomethacin for 28 days. The arthritic index and body weight were determined at regular intervals, together with hepatic, hematological, and antioxidant parameters. The expression of proinflammatory cytokines (e.g., IL-6, TNF-α, and IL-1β) and inflammatory mediators (e.g., COX-2 and VEGF) were also estimated with histopathological evaluation of the joint tissue of rats. A docking study of pinitol with PTPN22 was also carried out.ResultsThe CFA-induced model rats developed redness and nodules in the tail and front paws, and the arthritic control (AC) group rats showed similar symptoms, which were decreased by pinitol administration. The body weight of AC group rats was decreased, while pinitol-treated rats showed considerably increased body weight. Hematological, hepatic, and antioxidant parameters were altered by pinitol in a dose-dependent manner. Pinitol significantly decreased the elevated concentration of proinflammatory cytokines and inflammatory mediators, with improvement in histopathological condition. The docking study suggested that pinitol efficiently interacted with PTPN22 via Arg59, Tyr60, Leu106, and Lys138 by creating close interatomic hydrogen bonds and hydrophobic contacts.ConclusionsPinitol showed anti-arthritic effects via reduction of proinflammatory cytokines and inflammatory mediators via inhibition of PTPN22.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Pinitol Against Inflammatory Mediators of Rheumatoid Arthritis via Inhibition of Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22)

et al. 2017

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“…There are some reports evaluating muscle atrophy in murine models of arthritis. Ozawa et al demonstrated reduction about 20 % in skeletal muscle and in muscle weight in a model adjuvant‐induced arthritis (complete Freund's adjuvant, CFA). Hartog et al have described reduced weight and spontaneous locomotion in collagen‐induced arthritis (CIA), demonstrating generalized muscle loss.…”

Section: Introductionmentioning

confidence: 99%

Temporal development of muscle atrophy in murine model of arthritis is related to disease severity

Filippin

Teixeira

Viacava

et al. 2013

J cachexia sarcopenia muscle

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BackgroundRheumatoid arthritis (RA) is an inflammatory autoimmune disease of unknown etiology, affecting mainly the joint but also other tissues. RA patients usually present weakness and muscle atrophy, nonarticular manifestations of the disease. Although causing great impact, the understanding of muscle atrophy, its development, and the mechanisms involved is still very limited. The objective of this study is to evaluate the development of muscle atrophy in skeletal muscle of a murine model of arthritis.MethodsThe experimental murine model of collagen-induced arthritis (CIA) was used. DBA/1J mice were randomly divided into three groups: control (CO, n = 25), sham arthritis (SA, n = 25), and arthritis (CIA, n = 28), analyzed in different time points: 25, 35, and 45 days after the induction of arthritis. The arthritis development was followed by clinical scores and hind paw edema three times a week. The spontaneous exploratory locomotion and weight were evaluated weekly. In all time points, serum was collected before the death of the animals for cytokine analysis, and myofiber cross-sectional areas (CSA) of gastrocnemius (GA) and tibialis anterior (TA) skeletal muscles were evaluated.ResultsThe clinical parameters of arthritis progressively increased in CIA in all experimental times, demonstrating the greatest difference from other groups at 45 days after induction (clinical score: CO, 00 ± 00; SA, 1.00 ± 0.14; CIA, 3.28 ± 0.41 p > 0.05). The CIA animals had lower weights during all the experimentation periods with a difference of 6 % from CO at 45 days (p > 0.05). CIA animals also demonstrated progressive decrease in distance walked, with a reduction of 54 % in 35 and 74 % at 45 days. Cytokine analysis identified significant increase in IL-6 serum levels in CIA than CO and SA in all experimental times. CSA of the myofiber of GA and TA was decreased 26 and 31 % (p > 0.05) in CIA in 45 days after the induction of disease, respectively. There was significant and inverse correlation between the disease clinical score and myofiber CSA in 45 days (GA: r = −0.71; p = 0.021).ConclusionOur results point to a progressive development of muscle wasting, with premature onset arthritis. These observations are relevant to understand the development of muscle loss, as well as for the design of future studies trying to understand the mechanisms involved in muscle wasting. As far as we are concerned, this is the first study to evaluate the relation between disease score and muscle atrophy in a model of arthritis.Electronic supplementary materialThe online version of this article (doi:10.1007/s13539-013-0102-1) contains supplementary material, which is available to authorized users.

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“…A previous study reported that the weight of the limb muscle was decreased in complete Freund's adjuvant‐induced arthritic rats. Additionally, the cross‐sectional area of the muscle of the affected limb was smaller than that of the saline‐injected side in these animals, indicating that joint pathology may induce peri‐articular muscle adaptation . Oner and colleagues and Griggs et al.…”

Section: Discussionmentioning

confidence: 90%

Melatonin treatment combined with treadmill exercise accelerates muscular adaptation through early inhibition of CHOP‐mediated autophagy in the gastrocnemius of rats with intra‐articular collagenase‐induced knee laxity

Hong

Kim

Jin

et al. 2014

Journal of Pineal Research

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The purpose of this study was to determine the effects of melatonin intervention on gastrocnemius remodeling in rats with collagenase-induced knee instability. Type VII collagenase was injected into the right knee to induce joint laxity with cartilage destruction. Melatonin (MT; 10 mg/kg) injection was performed twice daily subcutaneously, and treadmill exercise (Ex; 11 m/min) was conducted for 1 hr/day at a frequency of 5 days/wk for 4 wks. The gastrocnemius mass, which was reduced with collagenase injection only (Veh), was increased with collagenase injection with melatonin treatment with and without exercise in the early phase, and the mass in both limbs was significantly different in the Veh compared with the MT group. However, there was an increase in the relative muscle weight to body weight ratio in the Veh group at the advanced stage. Insulin-like growth factor receptor (IGF-IR) was downregulated in the Veh group, whereas IGF-IR was upregulated in the MT and MT + Ex groups. Joint laxity induced enhancement of autophagic proteolysis (LC3 II) in the muscle, which was recovered to values similar to those in the normal control group (Con) compared with those in the MT and MT+Ex groups. Although intra-articular collagenase increased the total C/EBP homology protein (CHOP) levels at 1 wk and decreased them at 4 wks in the Veh group, CHOP in the nucleus was upregulated continuously. Prolonged melatonin treatment with and without exercise intervention suppressed nuclear localization of ATF4 and CHOP with less activation of caspase-3, at the advanced phase. Moreover, the interventions promoted the expression of myosin heavy chain (MHC) isoforms under the control of myogenin. Concomitant with a beneficial effect of melatonin with and without exercise, step length of the saline-injected limb and the collagenase-injected supporting side was maintained at values similar to those in control rats. Taken together, the findings demonstrate that melatonin with and without exercise accelerate remodeling of the gastrocnemius through inhibition of nuclear CHOP in rats with collagenase-induced knee instability.

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Morphological changes in hind limb muscles elicited by adjuvant‐induced arthritis of the rat knee

Cited by 13 publications

References 35 publications

Protective Effect of Pinitol Against Inflammatory Mediators of Rheumatoid Arthritis via Inhibition of Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22)

Protective Effect of Pinitol Against Inflammatory Mediators of Rheumatoid Arthritis via Inhibition of Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22)

Temporal development of muscle atrophy in murine model of arthritis is related to disease severity

Melatonin treatment combined with treadmill exercise accelerates muscular adaptation through early inhibition of CHOP‐mediated autophagy in the gastrocnemius of rats with intra‐articular collagenase‐induced knee laxity

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