-Gingerol induces bone loss in ovary intact adult mice and augments osteoclast function via the transient receptor potential vanilloid 1 channel
Article first published online: 4 OCT 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 56, Issue 12, pages 1860–1873, December 2012
How to Cite
Khan, K., Singh, A., Mittal, M., Sharan, K., Singh, N., Dixit, P., Sanyal, S., Maurya, R. and Chattopadhyay, N. (2012), -Gingerol induces bone loss in ovary intact adult mice and augments osteoclast function via the transient receptor potential vanilloid 1 channel. Mol. Nutr. Food Res., 56: 1860–1873. doi: 10.1002/mnfr.201200200
- Issue published online: 6 DEC 2012
- Article first published online: 4 OCT 2012
- Manuscript Accepted: 20 AUG 2012
- Manuscript Revised: 17 JUL 2012
- Manuscript Received: 6 APR 2012
- Ministry of Health and Family Welfare
- Government of India
- Bone histomorphometry;
- Bone safety;
- Estrogen deficiency;
- Vanilloid channels
-Gingerol, a major constituent of ginger, is considered to have several health beneficial effects. The effect of 6-gingerol on bone cells and skeleton of mice was investigated.
Methods and results
The effects of 6-gingerol on mouse bone marrow macrophages and osteoblasts were studied. 6-Gingerol-stimulated osteoclast differentiation of bone marrow macrophages but had no effect on osteoblasts. Capsazepine, an inhibitor of TRPV1 (transient receptor potential vanilloid 1) channel, attenuated the pro-osteoclastogenic effect of 6-gingerol or capsaicin (an agonist of TRPV1). Similar to capsaicin, 6-gingerol stimulated Ca2+ influx in osteoclasts. The effect of daily feeding of 6-gingerol for 5 wk on the skeleton of adult female Balb/cByJ mice was investigated. Mice treated with capsaicin and ovariectomized (OVx) mice served as controls for osteopenia. 6-Gingerol caused increase in trabecular osteoclast number, microarchitectural erosion at all trabecular sites and loss of vertebral stiffness, and these effects were comparable to capsaicin or OVx group. Osteoclast-specific serum and gene markers of 6-gingerol-treated mice were higher than the OVx group. Bone formation was unaffected by 6-gingerol.
Daily feeding of 6-gingerol to skeletally mature female mice caused trabecular osteopenia, and the mechanism appeared to be activation of osteoclast formation via the TRPV1 channel.