Abstract
ObjectiveThere 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.MethodsNinety 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.ResultsThe 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).ConclusionsThe 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.
Highlights
The important function of bone can be 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 serum levels of macrophage colony-stimulating factor (M-CSF) in E group rats were highest in the five groups at 4 and 8 weeks (411.85 ± 123.73 pg/ml versus 589.62 ± 147.85 pg/ml, respectively) and have significant difference compared to the other groups (P < 0.01)
The serum levels of receptor activator of NF-kappaB ligand (RANKL) in E group rats were highest at 4 weeks (0.228 ± 0.085 ng/ml), which have significant difference compared to the other groups at 4 weeks and compared to 8 or 12 week levels in E group (P < 0.01)
Summary
The important function of bone can be 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]. 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. Three main hypotheses for the etiology of KBD are considered to be selenium deficiency in food, hypoalimenation in food and severe contamination of food by fungal mycotoxins [11,12,13,14,15]. Cereal grain contamination by Fusarium spp. and Alternaria sp. In endemic areas of China, and cereal samples in high incidence areas of KBD were reported to be more heavily contaminated with trichotecenes (T-2 toxins) when compared to those in low incidence areas [19,20] Cereal grain contamination by Fusarium spp. and Alternaria sp. in endemic areas of China, and cereal samples in high incidence areas of KBD were reported to be more heavily contaminated with trichotecenes (T-2 toxins) when compared to those in low incidence areas [19,20]
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