Conflict of interest: None.
Glucosamine protects nucleus pulposus cells and induces autophagy via the mTOR-dependent pathway
Article first published online: 2 AUG 2014
© 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
Journal of Orthopaedic Research
Volume 32, Issue 11, pages 1532–1542, November 2014
How to Cite
Jiang, L., Jin, Y., Wang, H., Jiang, Y. and Dong, J. (2014), Glucosamine protects nucleus pulposus cells and induces autophagy via the mTOR-dependent pathway. J. Orthop. Res., 32: 1532–1542. doi: 10.1002/jor.22699
- Issue published online: 22 SEP 2014
- Article first published online: 2 AUG 2014
- Manuscript Accepted: 26 JUN 2014
- Manuscript Received: 17 JAN 2014
- Natural Science Foundation of China. Grant Number: 81372002
- Natural Science Foundation of China. Grant Number: 31170925
- “Technology Innovation Action Plan” Key Project of Shanghai Science and Technology Commission. Grant Number: 12411951300
- National Basic Research Program of China(973 program). Grant Number: 2009CB930002
- nucleus pulposus;
Although glucosamine has been suggested to be effective in the treatment of osteoarthritis, its effect on disc degeneration remains unclear. We sought to explore whether glucosamine can activate autophagy in rat nucleus pulposus (NP) cells and protect cells treated with IL-1β or hydrogen peroxide (H2O2). Autophagy in cells was examined by detecting for LC3, Beclin-1, m-TOR, and p70S6K, as well as by analyzing autophagosomes. To inhibit autophagy, 3-methyladenine (3-MA) was used. In the cells treated with IL-1β, the levels of Adamts-4, Mmp-13, aggrecan, and Col2a1 were analyzed by real-time PCR and immunofluorescence. Apoptosis was analyzed by TUNEL. Cell senescence under H2O2 was revealed by SA-β-Gal staining. Glucosamine could activate autophagy in a dose-dependent manner within 24 h and inhibit the phosphorylation of m-TOR and p70S6K. Autophagy in IL-1β or H2O2-treated cells was increased by glucosamine. Glucosamine attenuated the decrease of aggrecan and prevented the apoptosis of the NP cells induced by IL-1β, whereas 3-MA partly reversed these effects. The percentage of SA-β-Gal-positive cells induced by H2O2 treatment was decreased by glucosamine, accompanied by the decline of p70S6K phosphorylation. Glucosamine protects NP cells and up-regulates autophagy by inhibiting the m-TOR pathway, which might point a potential therapeutic agent for disc degeneration. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1532–1542, 2014.