Article Publish Status: FREE
Abstract Title:

Effects of emodin on inflammatory bowel diseases related osteoporosis.

Abstract Source:

Biosci Rep. 2020 Jan 14. Epub 2020 Jan 14. PMID: 31934719

Abstract Author(s):

Jing-Sheng Luo, Xinhua Zhao, Yu Yang

Article Affiliation:

Jing-Sheng Luo


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 this 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% 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 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.

Study Type : Animal Study

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