期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 16, 期 11, 页码 27470-27481出版社
MDPI AG
DOI: 10.3390/ijms161126039
关键词
andrographolide; osteoclastogenesis; RANKL; OVX; bone loss
资金
- Co-innovation Centre for Bio-Medicine, Guangxi colleges and universities Key Laboratory of Regenerative Medicine and Innovation Team of Tissue Repair and Reconstruction
- National Health and Medical Research Council of Australia
- National Natural Science Foundation of China (NSFC) [8122801]
- Innovation Program of Postgraduate Education in Guangxi [YCSZ2015112]
- Arthritis foundation of Australia
- University of Western Australia (UWA) Research Collaboration Awards
- Chinese Scholarship Council
Osteoporosis is a debilitating skeletal disorder with an increased risk of low-energy fracture, which commonly occurs among postmenopausal women. Andrographolide (AP), a natural product isolated from Andrographis paniculata, has been found to have anti-inflammatory, anti-cancer, anti-asthmatic, and neuro-protective properties. However, its therapeutic effect on osteoporosis is unknown. In this study, an ovariectomy (OVX) mouse model was used to evaluate the therapeutic effects of AP on post-menopausal osteoporosis by using micro-computed tomography (micro-CT). Bone marrow-derived osteoclast culture was used to examine the inhibitory effect of AP on osteoclastogenesis. Real time PCR was employed to examine the effect of AP on the expression of osteoclast marker genes. The activities of transcriptional factors NF-B and NFATc1 were evaluated using a luciferase reporter assay, and the IB protein level was analyzed by Western blot. We found that OVX mice treated with AP have greater bone volume (BV/TV), trabecular thickness (Tb.Th), and trabecular number (Tb.N) compared to vehicle-treated OVX mice. AP inhibited RANKL-induced osteoclastogenesis, the expression of osteoclast marker genes including cathepsin K (Ctsk), TRACP (Acp5), and NFATc1, as well as the transcriptional activities of NF-B and NFATc1. In conclusion, our results suggest that AP inhibits estrogen deficiency-induced bone loss in mice via the suppression of RANKL-induced osteoclastogensis and NF-B and NFATc1 activities and, thus, might have therapeutic potential for osteoporosis.
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