Serum levels of M-CSF, RANKL and OPG in rats fed with Kashin-Beck disease-affected diet
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RESEARCH ARTICLE
Open Access
Serum levels of M-CSF, RANKL and OPG in rats fed with Kashin-Beck disease-affected diet Denglu Yan1,2*, Fuxing Pei2 and Yancheng Song3
Abstract Objective: There were no studies on the macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) in the pathogenesis of Kashin-Beck disease (KBD). The objective of the present study was to investigate the serum M-CSF, RANKL and OPG in rats fed with KBD-affected diet. Methods: Ninety Wistar rats were divided into five groups. The rats received standard commercial feed with or without T-2 toxin additive, low protein feed with or without or T-2 toxin additive and the KBD-affected feed. The serum bioactivity of M-CSF, RANKL and OPG was tested by enzyme-linked immunosorbent assay. Results: The serum levels of M-CSF in E group rats were higher than those in the other groups in the five groups (P < 0.01). The serum levels of RANKL and OPG in E group rats were highest in the five groups and have significant difference compared to the other groups (P < 0.05). Conclusions: The molecule of M-CSF, RANKL and OPG may be involved in the regulation of epiphyseal plate injury and repair in KBD, and its participation in the pathogenesis of KBD should be studied in the future. Keywords: Kashin-Beck disease, Macrophage colony-stimulating factor, Osteoprotegerin ligand receptor activator of NF-kappaB ligand, Osteoprotegerin
Introduction The important function of bone can be easily recognized in day-to-day life, where millions of people suffer from bone disease such as osteoporosis, which is, in part, caused by an imbalance between bone formation and bone resorption [1,2]. The better understanding of the regulation of bone formation will provide new insights into the molecular mechanisms of Kashin-Beck disease (KBD), which usually afflicts children between the ages of 5 and 13 years with epiphyseal plates showing focal or irregular premature closure, wherein in the normal bone formation, endochondral ossification ends up about 20 years after birth in humans [3-5]. Its initial pathologic changes are multiple degenerative and necrotic lesions within the growth plate cartilage. The secondary pathologic findings, visible on radiographs, are repairing and remodeling around the necrotic foci of the cartilage of * Correspondence: [email protected] 1 Nanshan Hospital of Shenzhen University, Shenzhen 518052, People’s Republic of China 2 West China Hospital, Sichuan University, Chengdu 610065, People’s Republic of China Full list of author information is available at the end of the article
the metaphysis, bone end and epiphysis [6-9]. With the development of modern molecular biology technology, there has been a focus on serum biomarkers as tools in evaluating cartilage destruction [10]. However, there is little understanding of the expression of these biological molecules and the relationship with possible pathogenic factors of KBD. Based on epidemiological investigations, three main hypotheses for the etiology of
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