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

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.

KEYWORDS:

• Back pain
• fullerol
• inflammation
• intervertebral disc degeneration
• link N peptide

Declaration of interest

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the article.

Funding

We appreciate the funding support in part from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR057512 and RO1AR064792), and North American Spine Society.

Additional information

Funding

We appreciate the funding support in part from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR057512 and RO1AR064792), and North American Spine Society.