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Glucosamine protects nucleus pulposus cells and induces autophagy via the mTOR‐dependent pathway
Author(s) -
Jiang LiBo,
Jin YongLong,
Wang HuiRen,
Jiang YunQi,
Dong Jian
Publication year - 2014
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.22699
Subject(s) - autophagy , glucosamine , apoptosis , pi3k/akt/mtor pathway , chemistry , tunel assay , microbiology and biotechnology , aggrecan , phosphorylation , osteoarthritis , biochemistry , biology , medicine , pathology , articular cartilage , alternative medicine
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 (H 2 O 2 ). 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 H 2 O 2 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 H 2 O 2 ‐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 H 2 O 2 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.