Literature DB >> 28509587

Link protein N-terminal peptide and fullerol promote matrix production and decrease degradation enzymes in rabbit annulus cells.

Ching-Hua Yeh1,2, Dennis Chen1, Bayan Aghdasi1, Li Xiao1, Mengmeng Ding1, Li Jin1, Xudong Li1.   

Abstract

PURPOSE: Intervertebral disc degeneration is a major cause of back pain. Novel therapies for prevention or reversal of disc degeneration are needed. It is desirable for potential therapies to target both inflammation and matrix degeneration.
MATERIALS AND METHODS: The combined regenerative potential of link protein N-terminal peptide (LN) and fullerol on annulus fibrosus (AF) cells was evaluated in a 3D culture model.
RESULTS: Interleukin-1α (IL-1α)-induced AF cell degeneration was counteracted by fullerol, LN, and fullerol + LN, with the latter having the greatest effect on matrix production as evaluated by real-time polymerase chain reaction and glycosaminoglycan assay. IL-1α-induced increases in pro-inflammatory mediators (interleukin-6 and cyclooxygenase-2) and matrix metalloproteinases (MMP-1, -2, -9, and -13) were also counteracted by fullerol and LN.
CONCLUSION: Our data demonstrate that LN and fullerol individually, and in combination, promote matrix production and have anti-inflammatory and anti-catabolic effects on AF cells.

Entities:  

Keywords:  Back pain; fullerol; inflammation; intervertebral disc degeneration; link N peptide

Mesh:

Substances:

Year:  2017        PMID: 28509587      PMCID: PMC5690886          DOI: 10.1080/03008207.2017.1330333

Source DB:  PubMed          Journal:  Connect Tissue Res        ISSN: 0300-8207            Impact factor:   3.417


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