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Abdi, Elham, Najafipour, Hamid, Joukar, Siyavash, Dabiri, Shahriar, Esmaeli-Mahani, Saeed, Abbasloo, Elham, Houshmandi, Nasrin, Afsharipour, Abbas. (1396). Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model. سامانه مدیریت نشریات علمی, 15(1), 14-27.
Elham Abdi; Hamid Najafipour; Siyavash Joukar; Shahriar Dabiri; Saeed Esmaeli-Mahani; Elham Abbasloo; Nasrin Houshmandi; Abbas Afsharipour. "Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model". سامانه مدیریت نشریات علمی, 15, 1, 1396, 14-27.
Abdi, Elham, Najafipour, Hamid, Joukar, Siyavash, Dabiri, Shahriar, Esmaeli-Mahani, Saeed, Abbasloo, Elham, Houshmandi, Nasrin, Afsharipour, Abbas. (1396). 'Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model', سامانه مدیریت نشریات علمی, 15(1), pp. 14-27.
Abdi, Elham, Najafipour, Hamid, Joukar, Siyavash, Dabiri, Shahriar, Esmaeli-Mahani, Saeed, Abbasloo, Elham, Houshmandi, Nasrin, Afsharipour, Abbas. Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model. سامانه مدیریت نشریات علمی, 1396; 15(1): 14-27.

Expression of IGF-1, IL-27 and IL-35 Receptors in Adjuvant Induced Rheumatoid Arthritis Model

Iranian Journal of Immunology
مقاله 2، دوره 15، شماره 1، خرداد 2018، صفحه 14-27    اصل مقاله (827.85 K)
نوع مقاله: Original Article
نویسندگان
Elham Abdi1؛ Hamid Najafipour* 2؛ Siyavash Joukar2؛ Shahriar Dabiri3؛ Saeed Esmaeli-Mahani4؛ Elham Abbasloo5؛ Nasrin Houshmandi1؛ Abbas Afsharipour6
1Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
2Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences and Department of Physiology and Pharmacology, Kerman University of Medical Sciences, Kerman, Iran
3Pathology and Stem Cell Research Center, Kerman University of Medical Sciences, Kerman, Iran
4Department of Biology, Shahid Bahonar University, Kerman University of Medical Sciences, Kerman, Iran
5Endocrinology and Metabolism Research Center, Kerman University of Medical Sciences, Kerman, Iran
6Gastroenterology and Hepathology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
چکیده
Background: IGF-1 and certain other cytokines have been shown to exert inflammatory/anti-inflammatory roles in chronic joint diseases. Objective: To assess the effect of IGF-1, IL-27 and IL-35, their interaction and their receptor expression in a rheumatoid arthritis model. Methods: Freund’s adjuvant-induced chronic joint inflammation was operated on 160 male rats. Animals were divided into histopathology and receptor expression groups, each composed of 10 subgroups including; control, vehicle, IGF-1, IL-27, IL-35, their antagonists, IGF-1+IL-27 antagonist and IGF-1+IL-35 antagonist. After two weeks, vehicle or agonist/antagonists were injected into the joint space every other day until day 28 where joint histopathology was performed. The expression of IGF-1, IL-27 and IL-35 receptors were assessed by western blot analysis. Results: IGF-1 did not show pro- or anti- inflammatory functions; endogenous IL-27 and IL-35, on the other hand, exerted inflammatory effects. IL-27 and IL-35 antagonists exerted the highest anti-inflammatory effects. The total inflammation scores were 0.55 ± 0.06, 4.63 ± 0.40, 3.63 ± 0.60, 2.50 ± 0.38 and 1.63 ± 0.40 regarding control, vehicle, IGF-1 Ant., IL-27 Ant. and IL-35Ant., respectively. IGF-1 receptor expression was reduced in chronic joint inflammation and all three antagonists augmented the IGF-1 receptor expression. IL-27 and IL-35 receptors were up-regulated by chronic joint inflammation. Conclusion: Overall, the results demonstrated the pro-inflammatory role of endogenous IL-27 and IL-35 along with the over expression of their receptors in chronic joint inflammation. IL-27 and IL-35 antagonists exerted the most anti-inflammatory effects and increased IGF-1 receptor expression. These two antagonists may be potential agents for new treatment strategies in chronic joint inflammatory diseases.
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