Effects of sodium hyaluronate and triamcinolone acetonide on glucosaminoglycan metabolism in equine articular chondrocytes treated with interleukin-1

Elysia C. Schaefer Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Allison A. Stewart Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Sushmitha S. Durgam Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Christopher R. Byron Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Matthew C. Stewart Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Abstract

Objective—To determine whether the effects of a high–molecular-weight sodium hyaluronate alone or in combination with triamcinolone acetonide can mitigate chondrocyte glyocosaminoglycan (GAG) catabolism caused by interleukin (IL)-1 administration.

Sample Population—Chondrocytes collected from metacarpophalangeal joints of 10 horses euthanized for reasons unrelated to joint disease.

Procedures—Chondrocyte pellets were treated with medium (negative control), medium containing IL-1 only (positive control), or medium containing IL-1 with hyaluronic acid only (0.5 or 2.0 mg/mL), triamcinolone acetonide only (0.06 or 0.6 mg/mL), or hyaluronic acid (0.5 or 2.0 mg/mL) and triamcinolone acetonide (0.06 or 0.6 mg/mL) in combination. Chondrocyte pellets were assayed for newly synthesized GAG, total GAG content, total DNA content, and mRNA for collagen type II, aggrecan, and cyclooxygenase (COX)-2.

Results—High-concentration hyaluronic acid increased GAG synthesis, whereas high-concentration triamcinolone acetonide decreased loss of GAG into the medium. High concentrations of hyaluronic acid and triamcinolone acetonide increased total GAG content. There was no change in DNA content with either treatment. Triamcinolone acetonide reduced COX-2 mRNA as well as aggrecan and collagen type II expression. Treatment with hyaluronic acid had no effect on mRNA for COX-2, aggrecan, or collagen type II.

Conclusions and Clinical Relevance—Results indicated that high concentrations of hyaluronic acid or triamcinolone acetonide alone or in combination mitigated effects of IL-1 administration on GAG catabolism of equine chondrocytes.

Abstract

Objective—To determine whether the effects of a high–molecular-weight sodium hyaluronate alone or in combination with triamcinolone acetonide can mitigate chondrocyte glyocosaminoglycan (GAG) catabolism caused by interleukin (IL)-1 administration.

Sample Population—Chondrocytes collected from metacarpophalangeal joints of 10 horses euthanized for reasons unrelated to joint disease.

Procedures—Chondrocyte pellets were treated with medium (negative control), medium containing IL-1 only (positive control), or medium containing IL-1 with hyaluronic acid only (0.5 or 2.0 mg/mL), triamcinolone acetonide only (0.06 or 0.6 mg/mL), or hyaluronic acid (0.5 or 2.0 mg/mL) and triamcinolone acetonide (0.06 or 0.6 mg/mL) in combination. Chondrocyte pellets were assayed for newly synthesized GAG, total GAG content, total DNA content, and mRNA for collagen type II, aggrecan, and cyclooxygenase (COX)-2.

Results—High-concentration hyaluronic acid increased GAG synthesis, whereas high-concentration triamcinolone acetonide decreased loss of GAG into the medium. High concentrations of hyaluronic acid and triamcinolone acetonide increased total GAG content. There was no change in DNA content with either treatment. Triamcinolone acetonide reduced COX-2 mRNA as well as aggrecan and collagen type II expression. Treatment with hyaluronic acid had no effect on mRNA for COX-2, aggrecan, or collagen type II.

Conclusions and Clinical Relevance—Results indicated that high concentrations of hyaluronic acid or triamcinolone acetonide alone or in combination mitigated effects of IL-1 administration on GAG catabolism of equine chondrocytes.

Contributor Notes

Supported by USDA Animal Health & Disease funds.

Presented in abstract form at the American College of Veterinary Surgeons Forum, Chicago, October 2007, and at the American Association of Equine Practitioners Convention, Orlando, Fla, December 2007.

The authors thank Dr. Peter Constable for assistance with statistical analysis.

Address correspondence to Dr. Allison Stewart (aaw@illinois.edu).
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