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      Impact of type III collagen on monosodium iodoacetate-induced osteoarthritis in rats

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          Abstract

          Osteoarthritis (OA) is a degenerative chronic disease that affects various tissues surrounding the joints, such as the subchondral bone and articular cartilage. The purpose of the study was to investigate the impact of collagen type III (CIII; 10 mg/kg; p.o.) on OA evidenced by restoration of articular cartilage structural changes as well as inflammatory responses using an established rat model of OA. OA was induced in rats by a single intra-articular injection of monosodium iodoacetate (MIA) through the right knee of the rats. Oral administration of CIII was undergone for 14 consecutive days. Changes in joint volume were measured throughout the experiment period with one-week intervals. At the end of the experiment, the rats were placed in the activity cage, and their activities were counted. Oxidative stress and nitrosative biomarkers were assessed by measuring the serum levels of malondialdehyde (MDA), reduced glutathione (GSH) and nitric oxide (NOx). Moreover, inflammatory markers viz. interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis nuclear factor-alpha (TNF-α) were measured. In addition, radiographic analysis and histopathological examination of the rat's knee were performed. The results of the current study revealed that oral treatment of MIA-induced osteoarthritic rats with CIII (10 mg/kg) for two weeks showed a marked decrease in the joint volume which led eventually to a prominent increase in the motor activity. Furthermore, treatment with CIII restored the serum levels of MDA, GSH, NOx, IL-6, IL-1β and the TNF-α. Furthermore, CIII succeeded to ameliorate the detrimental effect of MIA on radiographic images and histopathological alterations of the joint. From these findings, it can be concluded that CIII has regenerative and anti-inflammatory properties, thus has the ability to counteract MIA-induced OA in rat. Finally, CIII is said to be a potential anti-osteoarthritic candidate.

          Abstract

          Monosodium iodoacetate; Osteoarthritis; Cartilage; Rats; Type III collagen; Nutrition; Musculoskeletal system; Pharmacology; Toxicology; Radiology.

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          Most cited references38

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          Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids.

          L Green, D A Wagner, J. Glogowski … (1982)
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            Pain-related sensory innervation in monoiodoacetate-induced osteoarthritis in rat knees that gradually develops neuronal injury in addition to inflammatory pain

            Sumihisa Orita, Tetsuhiro Ishikawa, Masayuki Miyagi … (2011)
            Background The exact mechanism of knee osteoarthritis (OA)-associated pain is unclear, whereas mixed evidence of inflammatory pain and neuropathic pain has been noted. We aimed to investigate pain-related sensory innervation in a monoiodoacetate (MIA)-induced model of OA. Methods Sixty of seventy female Sprague Dawley rats of six week-old underwent intra-articular MIA and fluorogold (FG) retrograde neurotracer injection into their right (ipsilateral) knee, while their left knees were treated with FG in saline as a control (contralateral knee). Other rats were treated with FG only bilaterally, and used as controls. Rats were evaluated for tactile allodynia using von Frey hairs. Proinflammatory mediators in the knee soft tissues, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and nerve growth factor (NGF), were quantified using ELISAs to evaluate inflammation in the knee after 1, 4, 7,14,21, and 28 days post injection:. Dorsal root ganglia (DRG) were immunostained for three molecules after 7,14,21, and 28 days post injection: calcitonin gene-related peptide (CGRP), a marker of inflammatory pain; and activating transcription factor-3 (ATF3) and growth associated protein-43 (GAP43), as markers for nerve injury and regenerating axons. The distribution of microglia in the spinal cord were also evaluated, because they have been reported to increase in neuropathic pain states. These evaluations were performed up to 28 days postinjection. P < 0.05 was considered significant. Results Progressive tactile allodynia and elevated cytokine concentrations were observed in ipsilateral knees. CGRP-immunoreactive (-ir) ipsilateral DRG neurons significantly increased, peaking at 14 days postinjection, while expression of FG-labeled ATF3-ir or ATF3-ir GAP43-ir DRG neurons significantly increased in a time-dependent manner. Significant proliferation of microglia were found with time in the ipsilateral dorsal horn. Conclusions Pain-related characteristics in a MIA-induced rat OA model can originate from an inflammatory pain state induced by the local inflammation initiated by inflammatory cytokines, and that state will be followed by gradual initiation of neuronal injury, which may induce the neuropathic pain state.
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              Sonography of the knee joint().

              A.A.K.A. Razek, N.S. Fouda, N Elmetwaley … (2009)
              The aim of this article is to review the sonographic appearances of common disorders involving the knee joint. Ultrasound is a sensitive method for diagnosis of tendon injuries. Injured ligaments appear swollen with mixed echogenicity. Meniscal injuries and muscle tears can be easily diagnosed. Ultrasound shows synovial thickening and effusion in inflammatory arthropathy and erosions of the articular surface in degenerative arthritis. It can be used effectively in the detection of rheumatoid arthritic activity and for grading degenerative arthritis lesions. Cystic lesions, as well as benign and malignant soft-tissue masses, are clearly delineated. Ultrasound is a safe noninvasive imaging modality that can be used for diagnosis of different disorders involving the knee joint.
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                Author and article information

                Contributors
                Gihan F. Asaad
                Journal
                Journal ID (nlm-ta): Heliyon
                Journal ID (iso-abbrev): Heliyon
                Title: Heliyon
                Publisher: Elsevier
                ISSN (Electronic): 2405-8440
                Publication date PMC-release: 07 June 2020
                Publication date Collection: June 2020
                Publication date (Electronic): 07 June 2020
                Volume: 6
                Issue: 6
                Electronic Location Identifier: e04083
                Affiliations
                [a ]Pharmacology Department, National Research Centre, 33 El Buhouth st-Dokki, Cairo Governorate 12622 Egypt
                [b ]Department of Pathology, Faculty of Veterinary Medicine, Cairo University Egypt
                Author notes
                [∗ ]Corresponding author. dr_g.asaad@ 123456yahoo.com
                Article
                Publisher ID: S2405-8440(20)30927-0 Publisher ID: e04083
                DOI: 10.1016/j.heliyon.2020.e04083
                PMC ID: 7284073
                PubMed ID: 32548322
                SO-VID: e56c9941-7ec1-4e92-8d5a-cfaada9aebba
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 1 May 2020
                Date revision received : 5 May 2020
                Date accepted : 22 May 2020
                Categories
                Subject: Article

                Keywords: monosodium iodoacetate,osteoarthritis,cartilage,rats,type iii collagen,nutrition,musculoskeletal system,pharmacology,toxicology,radiology
                Data availability:
                Keywords: monosodium iodoacetate, osteoarthritis, cartilage, rats, type iii collagen, nutrition, musculoskeletal system, pharmacology, toxicology, radiology

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