Emodin promotes the osteogenesis of MC3T3- E1 cells via BMP-9/Smad pathway and exerts a preventive effect in ovariectomized rats

• Published in: Acta biochimica et biophysica Sinica Vol. 49; no. 10; pp. 867 - 878
• Main Authors: Chen, Xiaojing, Zhang, Shuang, Chen, Xiaoting, Hu, Yan, Wu, Jin, Chen, Shuyan, Chang, Jing, Wang, Genfa, Gao, Yanhong
• Format: Journal Article
• Language: English
• Published: China 01.10.2017
• Subjects: Animals; Cell Differentiation - drug effects; Cell Differentiation - genetics; Cell Line; Emodin - chemistry; Emodin - pharmacology; Gene Expression - drug effects; Growth Differentiation Factor 2 - genetics; Growth Differentiation Factor 2 - metabolism; Mice; Molecular Structure; Osteoblasts - cytology; Osteoblasts - drug effects; Osteoblasts - metabolism; Osteocalcin - blood; Osteocalcin - metabolism; Osteogenesis - drug effects; Osteogenesis - genetics; Ovariectomy; p38丝裂原活化蛋白激酶; Protein Kinase Inhibitors - pharmacology; Rats, Sprague-Dawley; Signal Transduction - drug effects; Signal Transduction - genetics; Smad Proteins - genetics; Smad Proteins - metabolism; 信号通路; 去卵巢大鼠; 大黄素; 成骨细胞; 碱性磷酸酶活性; 防治; 骨形态发生蛋白; BMP-9/Smad pathway; estrogen; osteoblast; osteoporosis; emodin
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmx087

Emodin, a natural anthraquinone extracted from the Chinese herbs rhubarb and giant knotweed rhizome, has been reported to enhance osteoblast differentiation. However, the mechanisms underlying its ability to regulate osteogenesis are unclear. The objective of this study was to deter- mine the role of emodin in osteoblast function in vitro and its osteoprotective effect in vivo. Emodin enhanced the differentiation and mineralization of MC3T3-E1 cells, as evidenced by ele- vated alkaline phosphatase activity and increased number of mineralized nodules. In cultured osteoblasts, emodin significantly induced the mRNA expression of BMP-9which is one of the least studied but most osteogenic bone morphogenetic proteins （BMPs）. Furthermore, the bone mor- phogenetic protein receptor-Smad （BMPR-Smad） signaling axis and p38 mitogen activated protein kinase （p38 MAPK） were activated. The in vivo function of emodin were evaluated by assessing bone histomorphology, trabecular bone microarchitecture, mechanical properties of the skeleton, and serum parameters of bone turnover in ovariectomized （OVX） rats. Emodin combined with low-dose of estrogen improved trabecular bone microarchitecture in the fourth lumbar vertebra compared with low-dose estrogen alone and enhanced vertebral body strength. Moreover, emo- din suppressed the OVX-induced elevation of serum osteocalcin （OC）. In addition, there were few- er side effects on uterine hypertrophy with the combination therapy than with high-dose estrogen alone. However, emodin alone did not exert any osteoprotective effect. These results suggest that emodin may be a promising alternative agent for osteoporosis in combination therapy.