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INCREASED PRO‐INFLAMMATORY GENE EXPRESSION IN ANNULUS FIBROSUS CELLS EXPOSED TO OMEGA‐3 FATTY ACIDS: GP38.

Gwendolyn, Sowa1; Moore, Carolyn1; Liggon, Michael1; Coelho, Paulo J.1; Vo, Nam1; Balk, Judith1; Preuss, Harry2; Kang, James1

Spine Journal Meeting Abstracts: October 2011 - Volume - Issue - [no page #]
GENERAL POSTERS
Free

1University of Pittsburgh, Pittsburgh, US; 2Georgetown University, Washinton D.C., US

INTRODUCTION: Omega‐3 fatty acids, common nutritional supplements found in fish oils, have demonstrated effects on cartilage matrix homeostasis through decreased inflammatory mediators. Similarly, decreased systemic inflammatory mediators were noted in a clinical study of patients with high dietary omega‐3 fatty acids. In addition, case report level data suggest improvement in patients with disc degeneration and low back pain, raising the question of their effects on intervertebral disc cell inflammation.

METHODS: Annulus fibrosus (AF) cells were isolated from skeletally mature female New Zealand White rabbits and exposed to various concentrations of DHA or EPA (1uM, 10uM, 100uM) in the presence or in the absence of IL‐1beta (1 ng/ml). After 24 hours, gene expression of inflammatory markers was analyzed through RT‐PCR of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX‐2).

RESULTS: Cells exposed to 100 uM EPA or DHA resulted in increased cell death. Exposure to EPA at 1uM or 10uM resulted in increased expression of iNOS and COX‐2. Exposure to DHA at 1uM resulted in a small decrease in iNOS expression and increase in COX‐2 expression, whereas exposure to 10uM DHA resulted in increased expression of both iNOS and COX‐2. In cells not stimulated with IL‐1 beta, exposure to either EPA or DHA demonstrated increased COX‐2 gene expression, but not iNOS expression.

DISCUSSION: The observation of increased catabolic gene expression in response to DHA or EPA is intriguing in light of the literature demonstrating an anti‐inflammatory effect in other tissues. However, additional studies will be needed to establish the effects on overall inflammation and potential effects on disc matrix homeostasis.

© 2011 Lippincott Williams & Wilkins, Inc.