Abstract
Inflammatory bowel diseases (IBD) are related to bone loss. Emodin can influence the activity and differentiation of osteoblasts and osteoclasts. However, few studies have shown the effects of emodin on IBD-induced bone damage. The aim of the present study was to investigate the role of emodin in IBD-induced osteoporosis in an animal model. An IBD model in Sprague Dawley male rats was established by administering 2.5% dextran sulfate sodium (DSS) in the drinking water. Emodin was administered orally (30 mg/kg body weight) every other day starting in the third week for 9 weeks. Blood, colon and bone samples were obtained for biomarker assays and histological analysis. Bone biomechanical properties, microCT, metabolic biomarkers and bone histological changes were analyzed. The bone mass was significantly decreased, and the bone biomechanical properties and bone microstructure parameters of IBD rats were significantly worse than those of control rats (P<0.05). Tartrate resistant acid phosphatase staining also showed that the number of osteoclasts in bone in IBD rats were larger than that in bone in control rats. Emodin intervention abolished the changes in bone microstructure and biomechanical properties (P<0.05) induced by IBD. Osteoclast formation and serum C-terminal cross-linked peptide (CTX) and tumor necrosis factor α (TNF-α) were also inhibited by emodin (P<0.05). Emodin significantly abolished IBD-enhanced Traf6, NFATC1 and c-fos expression. Our data demonstrated that emodin suppresses IBD-induced osteoporosis by inhibiting osteoclast formation.
Highlights
Inflammatory bowel diseases (IBDs) are a common cause of chronic gastrointestinal lesions
We showed the therapeutic effectiveness of emodin for IBD-induced bone loss in an IBD model
Study in vivo indicated that natural compounds derived from herbs are applicable for the treatment of IBD-related osteoporosis [9]
Summary
Inflammatory bowel diseases (IBDs) are a common cause of chronic gastrointestinal lesions. The incidence of IBD increased in the 1990s. Systemic inflammation and extraintestinal manifestations are usually observed in IBD patients [1,2]. The pathogenic mechanism of IBD is still not clarified. Immune and environmental factors may all play critical roles in IBD [3]. Bone loss was observed in almost half of IBD patients [1]. The risk of bone fracture was relatively high in IBD patients. Systemic inflammation may be an etiological factor of bone loss in IBD patients. The cytokines released by inflammatory cells, like for example tumor necrosis factor α (TNF-α), can lead to mature osteoclast formation which causes excessive bone resorption and low bone mass [3]
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